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Gene Information
Gene symbol: POMC
Gene name: proopiomelanocortin
HGNC ID: 9201
Synonyms: MSH, POC, CLIP, ACTH, NPP, LPH
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 84999 | DAMME and other substances with opiate-like activity, such as morphine and beta-endorphin, affect carbohydrate metabolism and insulin secretion. |
| 2 | 140046 | The binding of labeled insulin was inhibited by low concentrations of unlabeled insulin and by high concentrations of proinsulin, whereas it was unaffected by the presence of glucagon, gastrin, prolactin, ACTH, or growth hormone in microgram amounts. |
| 3 | 168109 | Although acute insulin deficiency in intact rats produced the previously described increase in protein synthetic activity of free hepatic ribosomes and decrease in activity of hepatic bound ribosomes, these changes did not occur in Hx rats, even when Hx rats received replacement doses of thyroxine, ACTH, and growth hormone. |
| 4 | 169200 | Intestinal absorption of L-histidine as affected by insulin, diabetes, hydrocortisone, adrenocorticotrophic hormone (ACTH) and thyroxine has been studied. |
| 5 | 171948 | Plasma ACTH levels were not elevated during clinical adrenal insufficiency or after metyrapone administration but did respond normally to vasopressin and insulin-induced hypoglycemia. |
| 6 | 172321 | Endocrine studies of hypothalamic-pituitary function revealed completely impaired secretion of gonadotropin, growth hormone and anti-diuretic hormone, and possible partial impairment of adrenocorticotropic hormone secretion, while thyroid stimulating hormone secretion remained intact. |
| 7 | 172321 | Persistently elevated plasma levels of human prolactin were also demonstrated, which were unaffected by administration of either thyrotropin releasing hormone, l-DOPA or water loading, but suppressed significantly by CB-154, an ergot alkaloid. |
| 8 | 204828 | In three patients with diabetes and hyporeninemic hypoaldosteronism changes in renin activity, plasma aldosterone and cortisol were examined under various conditions: orthostasis and intravenous furosemide, infusion of synthetic beta1-24 ACTH on two consecutive days and diurnal variations in basal hormone fluctuations. |
| 9 | 205644 | We report five females with septo-optic dysplasia, blindness, and multiple pituitary tropic hormone deficiencies: all were growth hormone and adrenocorticotropic hormone deficient; two had diabetes insipidus; one had sexual precocity, and one had early pubertal maturation, whereas three were prepubertal and responded to administration of synthetic gonadotropin-releasing hormone. |
| 10 | 225167 | A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. |
| 11 | 225167 | His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. |
| 12 | 225167 | These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. |
| 13 | 425859 | After neurosurgical treatment GHD was present in all, hypothyroidism in five, ACTH-deficiency in three, hyperprolactinaemia in three, and diabetes insipidus in four children. |
| 14 | 425859 | From the data presented here one may suggest that TRH stimulation tests, evaluation of serum prolactin, and lysin-vasopressin stimulation tests are the most useful investigations to distinguish between hypothalamic and primary pituitary disorders. |
| 15 | 461384 | The diaphragm of hypophysectomized rats had an increased capacity to the C14-glucose uptake from the medium and of incorporating it into glycogen, apparently on account of exclusion of the hormones group depending on the hypophysis, with the contrainsular action (STH, ACTH, TTH). |
| 16 | 950364 | Dissociation of renin and aldosterone during dehydration: studies in a case of diabetes insipidus and adipsia. |
| 17 | 950364 | The abnormal aldosterone-renin ratio was probably not caused by an intrinsic adrenal abnormality, since high levels of aldosterone were measured as long as a certain degree of hydration had been achieved with or without exogenous ADH, and since plasma cortisol was normal and responsive to exogenous ACTH. |
| 18 | 989992 | Endocrine function tests were performed as follows: growth hormone (GH) was measured after insulin-induced-hypoglycaemia, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after LH-releasing hormone, thyrotrophin (TSH) and prolactin after thyrotrophin-releasing hormone; pituitary reserve of adrenocorticotrophin (ACTH) was determined by measurement of plasma cortisol after lysine-vasopressin and 11 deoxycortisol after metyrapone. |
| 19 | 989992 | Finally three cases of amenorrhoeagalactorrhoea, with normal prolactin level, and/or diabetes insipidus remained unexplained. |
| 20 | 1285360 | The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. |
| 21 | 1285360 | No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. |
| 22 | 1313174 | Immunohistochemical analysis of the tumor specimen demonstrated the presence of some neoplastic cells immunoreactive for chromogranin A, neuron-specific enolase and ACTH. |
| 23 | 1314697 | In the present study, binding of DAB389-MSH to melanotropin receptors in biopsy specimens of human and mouse melanoma metastases was assessed by measuring its ability to inhibit binding of a radiolabeled, superpotent analogue of alpha-MSH (125I-[Nle4,D-Phe7]-alpha-MSH; 125I-NDP-MSH) and comparing its potency in this system with those of the established ligands NDP-MSH and alpha-MSH. |
| 24 | 1314697 | Taken together, these results suggest that NDP-MSH, alpha-MSH, and DAB389-MSH bind to a common melanotropin receptor in human metastatic melanoma cells. |
| 25 | 1314697 | In the present study, binding of DAB389-MSH to melanotropin receptors in biopsy specimens of human and mouse melanoma metastases was assessed by measuring its ability to inhibit binding of a radiolabeled, superpotent analogue of alpha-MSH (125I-[Nle4,D-Phe7]-alpha-MSH; 125I-NDP-MSH) and comparing its potency in this system with those of the established ligands NDP-MSH and alpha-MSH. |
| 26 | 1314697 | Taken together, these results suggest that NDP-MSH, alpha-MSH, and DAB389-MSH bind to a common melanotropin receptor in human metastatic melanoma cells. |
| 27 | 1319562 | Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. |
| 28 | 1319562 | Postoperatively, the serum prolactin and corticotropin levels decreased significantly. |
| 29 | 1319562 | The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed. |
| 30 | 1319562 | Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. |
| 31 | 1319562 | Postoperatively, the serum prolactin and corticotropin levels decreased significantly. |
| 32 | 1319562 | The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed. |
| 33 | 1319562 | Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. |
| 34 | 1319562 | Postoperatively, the serum prolactin and corticotropin levels decreased significantly. |
| 35 | 1319562 | The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed. |
| 36 | 1332223 | While the adrenocorticotropic hormone (ACTH) concentrations of 10-53 pg/ml remained constant during the study period, thyroid-stimulating hormone (TSH) and human growth hormone (hGH) concentrations showed a 12- and 35-fold increase from baseline values after 30-40 hr. |
| 37 | 1333962 | During blockade with atropine the responses of plasma prolactin was reduced, with a slight but significant reduction in the growth hormone response, and although a similar maximum response of plasma ACTH was achieved, this rise was delayed. |
| 38 | 1338326 | The synergism between insulin and cortisol in stimulating energy deposition, associated with a decreased effect of corticotropin-releasing factor in stimulating energy expenditure, is likely to contribute to the development of obesity. |
| 39 | 1517373 | The ACTH and cortisol responses to CRH were normal in two, blunted in one, and suppressed in four patients. |
| 40 | 1518441 | Particularly in the ectopic growth hormone-releasing hormone (GHRH) syndrome, Sandostatin is unequivocally effective and, in the ectopic corticotropin syndrome selected cases can be treated successfully with Sandostatin, leading to marked clinical improvement. |
| 41 | 1591027 | We reported a 16-year-old boy suffering from dwarfism, diabetes insipidus and progressive cerebellar ataxia. |
| 42 | 1591027 | Pituitary hormones (GH and ACTH) sufficiently responded to the loading of hypothalamic hormones such as growth hormone releasing factor and corticotropin releasing factor, in spite of poor responses of GH under the insulin stimulation or sleep. |
| 43 | 1649812 | Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. |
| 44 | 1649812 | Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. |
| 45 | 1649812 | Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. |
| 46 | 1649812 | Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. |
| 47 | 1652435 | Once the diagnosis of Cushing's syndrome is made with certainty, an initial separation into ACTH-dependent versus ACTH-independent categories is made on the basis of the plasma ACTH response to CRH. |
| 48 | 1652435 | Patients with an ACTH-dependent process are then divided into eutopic versus ectopic sources on the basis of the central to peripheral gradient of ACTH measured in the inferior petrosal sinuses simultaneously 3 to 5 minutes after the administration of CRH, 1 microgram/kg. |
| 49 | 1652435 | Once the diagnosis of Cushing's syndrome is made with certainty, an initial separation into ACTH-dependent versus ACTH-independent categories is made on the basis of the plasma ACTH response to CRH. |
| 50 | 1652435 | Patients with an ACTH-dependent process are then divided into eutopic versus ectopic sources on the basis of the central to peripheral gradient of ACTH measured in the inferior petrosal sinuses simultaneously 3 to 5 minutes after the administration of CRH, 1 microgram/kg. |
| 51 | 1666347 | In view of the immune-mediated nature of Type 1 (insulin-dependent) diabetes mellitus, 49 recently diagnosed diabetic patients were investigated in terms of serum 1,25-(OH)2D3-levels, 25-hydroxyvitamin D3(25-(OH)D3), alpha-MSH and ACTH, and compared with 42 healthy controls. |
| 52 | 1666347 | No difference was found in the mean and median values of alpha-MSH and ACTH between IDDM patients and controls, although patients exhibited much higher variation of alpha-MSH levels than did controls. |
| 53 | 1666347 | In view of the immune-mediated nature of Type 1 (insulin-dependent) diabetes mellitus, 49 recently diagnosed diabetic patients were investigated in terms of serum 1,25-(OH)2D3-levels, 25-hydroxyvitamin D3(25-(OH)D3), alpha-MSH and ACTH, and compared with 42 healthy controls. |
| 54 | 1666347 | No difference was found in the mean and median values of alpha-MSH and ACTH between IDDM patients and controls, although patients exhibited much higher variation of alpha-MSH levels than did controls. |
| 55 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 56 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 57 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 58 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 59 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 60 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 61 | 1691431 | Marked sex differences in lean control mice were found at 3 weeks of age in pancreatic Met-enkephalin-LI and galanin-LI (with two- to threefold higher content in males). |
| 62 | 1691431 | Low pancreatic content (50% to 70% lower than in control mice) of galanin-LI, Met-enkephalin-LI and Leu-enkephalin-LI was associated with hyperinsulinemia in male B6 ob/ob and db/db mice at 3 weeks of age, though not in B6 db/db females and not in BKs db/db mice of either sex. |
| 63 | 1691431 | Marked sex differences in lean control mice were found at 3 weeks of age in pancreatic Met-enkephalin-LI and galanin-LI (with two- to threefold higher content in males). |
| 64 | 1691431 | Low pancreatic content (50% to 70% lower than in control mice) of galanin-LI, Met-enkephalin-LI and Leu-enkephalin-LI was associated with hyperinsulinemia in male B6 ob/ob and db/db mice at 3 weeks of age, though not in B6 db/db females and not in BKs db/db mice of either sex. |
| 65 | 1701038 | Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells. |
| 66 | 1701038 | When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased. |
| 67 | 1701038 | The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity. |
| 68 | 1701038 | Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially. |
| 69 | 1701038 | However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity. |
| 70 | 1701038 | Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone. |
| 71 | 1701038 | Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone. |
| 72 | 1701038 | Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells. |
| 73 | 1701038 | When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased. |
| 74 | 1701038 | The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity. |
| 75 | 1701038 | Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially. |
| 76 | 1701038 | However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity. |
| 77 | 1701038 | Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone. |
| 78 | 1701038 | Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone. |
| 79 | 1701038 | Colchicine treatment alone resulted in appearance of galanin-, dynorphin-, cholecystokinin-, [Leu]enkephalin- and thyrotropin-releasing hormone-positive cells. |
| 80 | 1701038 | When salt-loaded rats received colchicine, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity in addition increased, whereas galanin- and dynorphin-like immunoreactivity markedly decreased. |
| 81 | 1701038 | The Brattleboro rats resembled untreated rats, except their lack of vasopressin-like immunoreactivity, the marked increase in tyrosine hydroxylase-like immunoreactivity, and smaller increase in galanin- and dynorphin-like immunoreactivity. |
| 82 | 1701038 | Addition of colchicine to Brattleboro rats resulted in some distinct further changes in that dynorphin-like immunoreactivity decreased in some neurons and that [Leu]enkephalin-, corticotropin-releasing factor- and peptide histidine-isoleucine-like immunoreactivity increased substantially. |
| 83 | 1701038 | However, a marked difference in immunoreactive [Leu]enkephalin levels was observed with no difference in dynorphin-like immunoreactivity, and opposite changes in galanin-like immunoreactivity. |
| 84 | 1701038 | Vasopressin-containing neurons primarily express tyrosine hydroxylase, galanin, dynorphin, [Leu]enkephalin and peptide histidine-isoleucine, and to a minor extent cholecystokinin and thyrotropin-releasing hormone. |
| 85 | 1701038 | Oxytocin-containing neurons mainly have cholecystokinin and corticotropin-releasing factor, and to a minor extent galanin, dynorphin, [Leu]enkephalin and thyrotropin-releasing hormone. |
| 86 | 1790277 | In the hypothalamus-hypophysis study, reserves of thyrotropin (TSH), prolactin (PRL), gonadotropins (FSH and LH), growth hormone (GH), adrenocorticotropin (ACTH) and cortisol were assessed. |
| 87 | 1851181 | Lack of enhanced responsiveness of plasma 18-hydroxycorticosterone and aldosterone to adrenocorticotropin as well as to angiotensin-II during moderate sodium depletion in type II diabetic subjects with normoreninemia. |
| 88 | 1851181 | Responses of plasma aldosterone (PA) and its precursor steroids to alpha ACTH-(1-24) (85.2 nmol, iv) injection and graded angiotensin-II (AII) infusions (3.90 and 7.80 pmol/kg.min for 30 min at each dose) on both 170 and 100 mmol sodium intakes were assessed in 25 type II diabetic subjects with normoreninemia and 11 age-matched normal subjects. |
| 89 | 1851181 | These results indicate a lack of enhanced responsiveness of plasma 18-OHB and PA to both ACTH and AII during moderate sodium restriction in nonazotemic type II diabetic subjects with normoreninemia. |
| 90 | 1851181 | It appears that these subjects have selective unresponsiveness of adrenal zona glomerulosa to sodium depletion per se, but not to ACTH or AII. |
| 91 | 1851181 | Lack of enhanced responsiveness of plasma 18-hydroxycorticosterone and aldosterone to adrenocorticotropin as well as to angiotensin-II during moderate sodium depletion in type II diabetic subjects with normoreninemia. |
| 92 | 1851181 | Responses of plasma aldosterone (PA) and its precursor steroids to alpha ACTH-(1-24) (85.2 nmol, iv) injection and graded angiotensin-II (AII) infusions (3.90 and 7.80 pmol/kg.min for 30 min at each dose) on both 170 and 100 mmol sodium intakes were assessed in 25 type II diabetic subjects with normoreninemia and 11 age-matched normal subjects. |
| 93 | 1851181 | These results indicate a lack of enhanced responsiveness of plasma 18-OHB and PA to both ACTH and AII during moderate sodium restriction in nonazotemic type II diabetic subjects with normoreninemia. |
| 94 | 1851181 | It appears that these subjects have selective unresponsiveness of adrenal zona glomerulosa to sodium depletion per se, but not to ACTH or AII. |
| 95 | 1851181 | Lack of enhanced responsiveness of plasma 18-hydroxycorticosterone and aldosterone to adrenocorticotropin as well as to angiotensin-II during moderate sodium depletion in type II diabetic subjects with normoreninemia. |
| 96 | 1851181 | Responses of plasma aldosterone (PA) and its precursor steroids to alpha ACTH-(1-24) (85.2 nmol, iv) injection and graded angiotensin-II (AII) infusions (3.90 and 7.80 pmol/kg.min for 30 min at each dose) on both 170 and 100 mmol sodium intakes were assessed in 25 type II diabetic subjects with normoreninemia and 11 age-matched normal subjects. |
| 97 | 1851181 | These results indicate a lack of enhanced responsiveness of plasma 18-OHB and PA to both ACTH and AII during moderate sodium restriction in nonazotemic type II diabetic subjects with normoreninemia. |
| 98 | 1851181 | It appears that these subjects have selective unresponsiveness of adrenal zona glomerulosa to sodium depletion per se, but not to ACTH or AII. |
| 99 | 1851181 | Lack of enhanced responsiveness of plasma 18-hydroxycorticosterone and aldosterone to adrenocorticotropin as well as to angiotensin-II during moderate sodium depletion in type II diabetic subjects with normoreninemia. |
| 100 | 1851181 | Responses of plasma aldosterone (PA) and its precursor steroids to alpha ACTH-(1-24) (85.2 nmol, iv) injection and graded angiotensin-II (AII) infusions (3.90 and 7.80 pmol/kg.min for 30 min at each dose) on both 170 and 100 mmol sodium intakes were assessed in 25 type II diabetic subjects with normoreninemia and 11 age-matched normal subjects. |
| 101 | 1851181 | These results indicate a lack of enhanced responsiveness of plasma 18-OHB and PA to both ACTH and AII during moderate sodium restriction in nonazotemic type II diabetic subjects with normoreninemia. |
| 102 | 1851181 | It appears that these subjects have selective unresponsiveness of adrenal zona glomerulosa to sodium depletion per se, but not to ACTH or AII. |
| 103 | 1963254 | Argyrophil and beta-endorphin immunoreactive cells in focal islet-cell adenomatosis and insulin-producing islet-cell adenomata. |
| 104 | 1963621 | To ascertain whether the dawn phenomenon occurs in normal adolescents and, if so, to determine its mechanism, we measured nocturnal plasma glucose, insulin, glucagon, growth hormone, cortisol, and adrenocorticotropic hormone (ACTH) levels between 01.00 and 08.00 h in 10 healthy adolescents. |
| 105 | 1963621 | ACTH correlated with MCRI (r = 0.66; p = 0.002) and prehepatic insulin secretion (r = 0.75; p less than 0.01). |
| 106 | 1963621 | To ascertain whether the dawn phenomenon occurs in normal adolescents and, if so, to determine its mechanism, we measured nocturnal plasma glucose, insulin, glucagon, growth hormone, cortisol, and adrenocorticotropic hormone (ACTH) levels between 01.00 and 08.00 h in 10 healthy adolescents. |
| 107 | 1963621 | ACTH correlated with MCRI (r = 0.66; p = 0.002) and prehepatic insulin secretion (r = 0.75; p less than 0.01). |
| 108 | 1966250 | As it's well known from the clinic, human syndromes depending on pituitary GH, ACTH and PRL secreting tumors are associated with alteration of glucose homeostasis. |
| 109 | 2167193 | Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. |
| 110 | 2167193 | In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. |
| 111 | 2167193 | Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. |
| 112 | 2167193 | Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. |
| 113 | 2167193 | In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. |
| 114 | 2167193 | Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. |
| 115 | 2167193 | Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. |
| 116 | 2167193 | In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. |
| 117 | 2167193 | Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. |
| 118 | 2172669 | The plasma levels of the following hormones were measured: basal thyroxine (T4), estradiol and cortisol; and also follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and adrenocorticotropic hormone (ACTH), basally and after acute challenge with LH releasing hormone (LHRH), GRF (1-29)NH2 or insulin hypoglycemia, TSH releasing hormone (TRH) and lysine-8-vasopressin, respectively. |
| 119 | 2216273 | Thyrotropin-releasing hormone and ACTH stimulation tests were also abnormal, requiring the institution of thyroid and cortisol replacement therapy. |
| 120 | 2226124 | A follow-up of nine of the hyperglycaemic cases showed a significant decline in beta-endorphin and insulin levels with recovery. |
| 121 | 2232625 | The aim of the study was to investigate the influence of 40 mg of the beta-blocker penbutolol (Betapressin TM; Hoechst Ltd., Frankfurt/Main) in comparison to placebo on the insulin consumption on the blood sugar profile in twelve insulin-dependent diabetes (IDDM) patients. |
| 122 | 2232625 | The same was also true for hormonal parameters as STH, ACTH, cortisol, and catecholamines. |
| 123 | 2233277 | In contrast, db/db mice of both C57BL/6J and C57BL/KsJ strains exhibited alterations in a total of four peptides in three brain areas: lower concentration of somatostatin-LI in median eminence, higher Met-enkephalin-LI in dorsal vagal complex of the medulla oblongata, higher substance P-LI and lower vasoactive intestinal polypeptide (VIP)-LI in amygdala. |
| 124 | 2480454 | In the hypothalamus and in the striatum of diabetic rats, there are significant higher levels of substance P and met-enkephalin, respectively. |
| 125 | 2480454 | Conversely, in the lumbar cord of diabetic animals, the levels of substance P and met-enkephalin are significantly reduced. |
| 126 | 2480454 | In the hypothalamus and in the striatum of diabetic rats, there are significant higher levels of substance P and met-enkephalin, respectively. |
| 127 | 2480454 | Conversely, in the lumbar cord of diabetic animals, the levels of substance P and met-enkephalin are significantly reduced. |
| 128 | 2502884 | Experiments on rats using the primary monolayer culture of isolated islet cells proved that insulin secretion is directly modulated by the growth hormone (GH), C-terminal tetrapeptide of cholecystokinin, thyroliberin, and met-enkephalin, and by certain blood plasma factors of diabetes I patients. |
| 129 | 2502884 | The blood plasma factors of IdDM patients influence the islets of Langerhans activity by either stimulating or depressing the secretory function of insulin producing cells. |
| 130 | 2513414 | Concomitantly with such transductional alteration detected in chronic diabetes, we observed a marked increase of the striatal content of met-enkephalin, which is known to utilize Gi/Go proteins for inhibition of adenylate cyclase. |
| 131 | 2523766 | Changes in met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary in diabetic rats: effects of insulin therapy. |
| 132 | 2523766 | Immunoreactive (IR)-met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary were measured in alloxan-diabetic rats with or without insulin treatment. 2. |
| 133 | 2523766 | Changes in met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary in diabetic rats: effects of insulin therapy. |
| 134 | 2523766 | Immunoreactive (IR)-met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary were measured in alloxan-diabetic rats with or without insulin treatment. 2. |
| 135 | 2527831 | Immunoreactive beta-endorphin and met- and leu-enkephalin contents in pancreas and pituitary of corpulent (cp/cp) rats. |
| 136 | 2527831 | In the present study, content of three opioid peptide immunoreactivities (beta-endorphin, met-enkephalin and leu-enkephalin) were measured in pituitary and pancreas of two recently described, genetically obese rats, the LA/N-cp and the SHR/N-cp. |
| 137 | 2527831 | There were no significant differences in content of immunoreactive beta-endorphin, met-enkephalin or leu-enkephalin in whole pituitary, posterior or anterior lobes of the pituitary, or pancreas which could be ascribed to the effect of the obese phenotype. |
| 138 | 2527831 | Immunoreactive beta-endorphin and met- and leu-enkephalin contents in pancreas and pituitary of corpulent (cp/cp) rats. |
| 139 | 2527831 | In the present study, content of three opioid peptide immunoreactivities (beta-endorphin, met-enkephalin and leu-enkephalin) were measured in pituitary and pancreas of two recently described, genetically obese rats, the LA/N-cp and the SHR/N-cp. |
| 140 | 2527831 | There were no significant differences in content of immunoreactive beta-endorphin, met-enkephalin or leu-enkephalin in whole pituitary, posterior or anterior lobes of the pituitary, or pancreas which could be ascribed to the effect of the obese phenotype. |
| 141 | 2527831 | Immunoreactive beta-endorphin and met- and leu-enkephalin contents in pancreas and pituitary of corpulent (cp/cp) rats. |
| 142 | 2527831 | In the present study, content of three opioid peptide immunoreactivities (beta-endorphin, met-enkephalin and leu-enkephalin) were measured in pituitary and pancreas of two recently described, genetically obese rats, the LA/N-cp and the SHR/N-cp. |
| 143 | 2527831 | There were no significant differences in content of immunoreactive beta-endorphin, met-enkephalin or leu-enkephalin in whole pituitary, posterior or anterior lobes of the pituitary, or pancreas which could be ascribed to the effect of the obese phenotype. |
| 144 | 2537845 | Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome. |
| 145 | 2537845 | Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. |
| 146 | 2537845 | This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. |
| 147 | 2537845 | Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome. |
| 148 | 2537845 | Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome. |
| 149 | 2537845 | Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. |
| 150 | 2537845 | This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. |
| 151 | 2537845 | Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome. |
| 152 | 2537845 | Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome. |
| 153 | 2537845 | Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. |
| 154 | 2537845 | This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. |
| 155 | 2537845 | Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome. |
| 156 | 2537845 | Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome. |
| 157 | 2537845 | Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. |
| 158 | 2537845 | This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. |
| 159 | 2537845 | Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome. |
| 160 | 2544774 | The 125I-ANF binding to retinal particulate preparations was not inhibited by 1 microM concentration of somatostatin, vasopressin, vasoactive intestinal peptide, adrenocorticotropin, thyrotropin releasing hormone, or leu-enkephalin. |
| 161 | 2545066 | Plasma 18-hydroxycorticosterone and aldosterone responses to angiotensin II and corticotropin in diabetic patients with hyporeninemic and normoreninemic hypoaldosteronism. |
| 162 | 2546964 | Effect of administration of corticotropin-releasing hormone and glucocorticoid on arginine vasopressin response to osmotic stimulus in normal subjects and patients with hypocorticotropinism without overt diabetes insipidus. |
| 163 | 2546964 | We examined the effect of CRH administration on the response of plasma arginine vasopressin (AVP) induced by an osmotic stimulus in six normal subjects and five patients with hypocorticotropinism without overt diabetes insipidus (four patients with Sheehan's syndrome and one with idiopathic pituitary dwarfism with ACTH deficiency). |
| 164 | 2546964 | Based on the relatively low plasma AVP response to the osmotic stimulus in patients and their lower plasma AVP levels and higher plasma osmolality under basal conditions, we suggest that patients with hypocorticotropinism have partial diabetes insipidus, in which impairment of central CRH action might be, at least in part, involved. |
| 165 | 2565915 | Suppression of ectopic adrenocorticotropin secretion by the long-acting somatostatin analog octreotide. |
| 166 | 2565915 | The long-acting somatostatin analog (octreotide) was administered to a 37-yr-old woman with the ectopic ACTH syndrome. |
| 167 | 2565915 | Suppression of ectopic adrenocorticotropin secretion by the long-acting somatostatin analog octreotide. |
| 168 | 2565915 | The long-acting somatostatin analog (octreotide) was administered to a 37-yr-old woman with the ectopic ACTH syndrome. |
| 169 | 2593179 | Substance P and met-enkephalin content are remarkably reduced throughout the small intestine, whereas vasoactive intestinal polypeptide levels (VIP) are significantly increased in the duodenum. |
| 170 | 2747219 | Dystrophic axons contained substance P- and gastrin-releasing peptide (gastrin-releasing peptide/bombesin)-like staining but were not labeled by antisera directed against vasoactive intestinal peptide, dynorphin-B, somatostatin, leu- and met-enkephalin and neuropeptide tyrosine. |
| 171 | 2747219 | Substance P and gastrin-releasing peptide/bombesin containing subpopulations of presynaptic elements in prevertebral sympathetic ganglia are thought to participate in local reflex control of bowel motility and lesions preferentially involving these elements may contribute to bowel dysfunction. |
| 172 | 2805586 | Analysis of the pro-opiomelanocortin gene in non-insulin dependent diabetic families. |
| 173 | 2805586 | Products of the pro-opiomelanocortin gene have been shown to have marked effects on insulin secretion. |
| 174 | 2805586 | Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. |
| 175 | 2805586 | Inherited defects in or near the pro-opiomelanocortin gene locus are unlikely to be directly involved in the aetiology of non-insulin dependent diabetes. |
| 176 | 2805586 | Analysis of the pro-opiomelanocortin gene in non-insulin dependent diabetic families. |
| 177 | 2805586 | Products of the pro-opiomelanocortin gene have been shown to have marked effects on insulin secretion. |
| 178 | 2805586 | Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. |
| 179 | 2805586 | Inherited defects in or near the pro-opiomelanocortin gene locus are unlikely to be directly involved in the aetiology of non-insulin dependent diabetes. |
| 180 | 2805586 | Analysis of the pro-opiomelanocortin gene in non-insulin dependent diabetic families. |
| 181 | 2805586 | Products of the pro-opiomelanocortin gene have been shown to have marked effects on insulin secretion. |
| 182 | 2805586 | Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. |
| 183 | 2805586 | Inherited defects in or near the pro-opiomelanocortin gene locus are unlikely to be directly involved in the aetiology of non-insulin dependent diabetes. |
| 184 | 2805586 | Analysis of the pro-opiomelanocortin gene in non-insulin dependent diabetic families. |
| 185 | 2805586 | Products of the pro-opiomelanocortin gene have been shown to have marked effects on insulin secretion. |
| 186 | 2805586 | Selective antagonists of beta-endorphin have been reported to correct the impaired insulin secretory response to glucose seen in non-insulin dependent diabetes. |
| 187 | 2805586 | Inherited defects in or near the pro-opiomelanocortin gene locus are unlikely to be directly involved in the aetiology of non-insulin dependent diabetes. |
| 188 | 2811647 | In several patients stimulation test with specific releasing factors (TRH, LHRH, oCRH) were carried out. |
| 189 | 2811647 | The maintained response of ACTH to CRH (even increased after acute withdrawal therapy) indicated that AVP is not necessary to ensure normal function to the CRH-ACTH axis. |
| 190 | 2825930 | To determine whether or not prolactin, as well as ACTH, was involved in the control of adrenal weight and steroid release, lesions in the median eminence which had previously resulted in impaired steroid release and atrophy of the adrenal were placed in animals in which the plasma prolactin was allowed to rise as a result of the lesions or prevented from rising by the administration of the dopamine agonist, CB-154. |
| 191 | 2834429 | Plasma beta-endorphin, free fatty acids and blood lipid changes in type 2 (non-insulin dependent) diabetic patients. |
| 192 | 2834429 | Plasma beta EP, together with plasma beta-lipotropin (beta LPH), ACTH, cortisol and plasma insulin (IRI), was measured by RIA after silicic acid plasma extraction and Sephedex G-75 column chromatography. |
| 193 | 2834429 | Plasma beta-endorphin, free fatty acids and blood lipid changes in type 2 (non-insulin dependent) diabetic patients. |
| 194 | 2834429 | Plasma beta EP, together with plasma beta-lipotropin (beta LPH), ACTH, cortisol and plasma insulin (IRI), was measured by RIA after silicic acid plasma extraction and Sephedex G-75 column chromatography. |
| 195 | 2836651 | Stimulation by hCRF of C-peptide release in type 2 diabetics during concomitant opioid receptor blockade. |
| 196 | 2836651 | Administration of synthetic human corticotropin-releasing factor (hCRF, 2 micrograms/kg body weight) during simultaneous application of the opioid antagonist naloxone (1.6 mg i.v. bolus, followed by an infusion at a rate of 1.2 mg/h) produced a significant increase in plasma C-peptide levels of six male Type 2 diabetic patients which even exceeded the postprandial values. |
| 197 | 2836651 | Such a mechanism may underlie the stimulatory action of hCRF/naloxone on B cells and would explain the absent reaction of peripheral venous plasma C-peptide to hCRF alone as well as the amplifying effect of simultaneous opioid receptor blockade. |
| 198 | 2840794 | In the present study, basal serum cortisol and ACTH levels were measured in normoprolactinemic amenorrheic patients with (N = 14) and without (N = 7) insulin-dependent diabetes mellitus. |
| 199 | 2844109 | Pituitary function was assessed by evaluating basal ACTH concentrations and results of a growth hormone stimulation test before and 1 and 12 weeks after hypophysectomy, an ACTH stimulation test, a thyrotropin-releasing hormone-stimulation test, and a modified water deprivation/vasopressin response test before and 1, 4, 8, and 12 weeks after hypophysectomy. |
| 200 | 2846679 | A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. |
| 201 | 2848001 | Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog. |
| 202 | 2848001 | Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. |
| 203 | 2848001 | Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog. |
| 204 | 2848001 | Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. |
| 205 | 2851469 | To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. |
| 206 | 2851469 | The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). |
| 207 | 2851469 | To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. |
| 208 | 2851469 | The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). |
| 209 | 2863707 | Increased plasma levels of immunoreactive beta-endorphin and corticotropin in non-insulin-dependent diabetes. |
| 210 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 211 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 212 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 213 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 214 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 215 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 216 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 217 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 218 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 219 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 220 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 221 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 222 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 223 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 224 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 225 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 226 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 227 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 228 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 229 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 230 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 231 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 232 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 233 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 234 | 2866128 | The effect of met-enkephalin and naloxone on somatostatin and insulin secretion from the isolated, perfused rat pancreas. |
| 235 | 2866128 | The effect of met-enkephalin and the opiate antagonist, naloxone, on somatostatin and insulin secretion from the isolated, perfused rat pancreas has been studied during perfusion with 300 mg/dl glucose. |
| 236 | 2866128 | In response to a gradient of met-enkephalin from 0 to 10(-5) M, release of somatostatin was inhibited at low concentrations and stimulated at high concentrations. |
| 237 | 2866128 | A gradient of met-enkephalin from 0 to 10(-6) M caused only an inhibition of somatostatin release, whereas insulin release was stimulated. |
| 238 | 2866128 | The effects of met-enkephalin on somatostatin release were antagonized by naloxone (10(-6) M). |
| 239 | 2866128 | Naloxone (10(-6) M) alone changed the endocrine secretions by decreasing somatostatin release and by stimulating insulin release. |
| 240 | 2866209 | Hyperglycaemia lasting for hours, has been produced in unanesthetized cats, rabbits and rats by injection into the cerebral ventricles or the cisterna magna of a variety of drugs (morphine, etorphine, pethidine, beta-endorphin, enkephalin, bombesin, TRH, cholecystokinin, naloxone, propranolol, phentolamine, chloralose, magnesium chloride and GABA). |
| 241 | 2870337 | Plasma immunoreactive beta-endorphin in non-insulin-dependent diabetes. |
| 242 | 2890560 | Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin. |
| 243 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 244 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 245 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 246 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 247 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 248 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 249 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 250 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 251 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 252 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 253 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 254 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 255 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 256 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 257 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 258 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 259 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 260 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 261 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 262 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 263 | 2896134 | The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. |
| 264 | 2896134 | Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). |
| 265 | 2896134 | When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. |
| 266 | 2896134 | In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. |
| 267 | 2896134 | Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid. |
| 268 | 2905198 | Immunohistologic localization of tyrosine hydroxylase (TOH), dopamine-beta-hydroxylase (DBH) and selected neuropeptides (vasoactive intestinal polypeptide, gastrin-releasing peptide (GRP)/bombesin, substance P, Leu-enkephalin, Met-enkephalin, dynorphin B, neuropeptide Y (NPY), somatostatin) was used to investigate the innervation of the small bowel in a rat model of diabetic autonomic neuropathy. |
| 269 | 2935473 | The effect of 5-hydroxytryptamine (5-HT) alteration on brain dopamine (DA), norepinephrine (NE), beta-endorphin (beta E) and immunoreactive insulin (IRI) was studied in Sprague-Dawley diabetic and control rats. |
| 270 | 2935473 | PCPA treatment significantly decreased brain content of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) while it caused significant increase and decrease in brain beta E and insulin levels, respectively, in both normal and diabetic rat. |
| 271 | 2935473 | Meanwhile, the administration of fluoxetine resulted in significant increase in brain content of 5-HT, DA, NE and insulin but significant decline of beta E in diabetic and saline control rats. |
| 272 | 2935473 | The results of this experiment indicate that 5-HT may be regulating both beta E and insulin regardless of the availability of pancreatic insulin. |
| 273 | 2935694 | Beta-endorphin concentrations in the hypothalamus, pituitary and plasma of streptozotocin-diabetic rats with and without insulin substitution therapy. |
| 274 | 2944783 | We have recently shown that in addition to beta-endorphin the opioid peptides Met- and Leu-enkephalin and their apparent precursors are localized in islet endocrine cells of the rat pancreas. |
| 275 | 2944783 | Elevations or decreases (P less than .05) were found in db/db mice (vs. lean littermates) as follows: pituitary content of Met-enkephalin was twofold higher at all ages studied; pituitary free Leu-enkephalin was lower at 4 wk and reversed to higher at 6-30 wk; pancreatic beta-endorphin was 30% lower at 4 wk and reversed to threefold higher at 6-12 wk; Met- and Leu-enkephalin-containing larger peptides were elevated at one or more points between 6 and 12 wk in both the pancreas and the pituitary. |
| 276 | 2944783 | Thus, the onset of overt obesity between 4 and 6 wk of age was accompanied by a marked rise in both pancreatic beta-endorphin and pituitary Leu-enkephalin; similar elevations in these parameters have been reported previously in C57BL/6J ob/ob mice at approximately 12 wk of age. |
| 277 | 2944783 | We have recently shown that in addition to beta-endorphin the opioid peptides Met- and Leu-enkephalin and their apparent precursors are localized in islet endocrine cells of the rat pancreas. |
| 278 | 2944783 | Elevations or decreases (P less than .05) were found in db/db mice (vs. lean littermates) as follows: pituitary content of Met-enkephalin was twofold higher at all ages studied; pituitary free Leu-enkephalin was lower at 4 wk and reversed to higher at 6-30 wk; pancreatic beta-endorphin was 30% lower at 4 wk and reversed to threefold higher at 6-12 wk; Met- and Leu-enkephalin-containing larger peptides were elevated at one or more points between 6 and 12 wk in both the pancreas and the pituitary. |
| 279 | 2944783 | Thus, the onset of overt obesity between 4 and 6 wk of age was accompanied by a marked rise in both pancreatic beta-endorphin and pituitary Leu-enkephalin; similar elevations in these parameters have been reported previously in C57BL/6J ob/ob mice at approximately 12 wk of age. |
| 280 | 2944783 | We have recently shown that in addition to beta-endorphin the opioid peptides Met- and Leu-enkephalin and their apparent precursors are localized in islet endocrine cells of the rat pancreas. |
| 281 | 2944783 | Elevations or decreases (P less than .05) were found in db/db mice (vs. lean littermates) as follows: pituitary content of Met-enkephalin was twofold higher at all ages studied; pituitary free Leu-enkephalin was lower at 4 wk and reversed to higher at 6-30 wk; pancreatic beta-endorphin was 30% lower at 4 wk and reversed to threefold higher at 6-12 wk; Met- and Leu-enkephalin-containing larger peptides were elevated at one or more points between 6 and 12 wk in both the pancreas and the pituitary. |
| 282 | 2944783 | Thus, the onset of overt obesity between 4 and 6 wk of age was accompanied by a marked rise in both pancreatic beta-endorphin and pituitary Leu-enkephalin; similar elevations in these parameters have been reported previously in C57BL/6J ob/ob mice at approximately 12 wk of age. |
| 283 | 2951394 | Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. |
| 284 | 2951394 | To address the possibility that an abnormality in pancreatic beta-endorphin activity might contribute to abnormal insulin secretion in diabetes mellitus, we studied the effects of beta-endorphin infusion on islet function in diabetic patients. |
| 285 | 2951394 | The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. |
| 286 | 2951394 | Acute insulin and glucagon responses to arginine were not increased by beta-endorphin, suggesting that the effect of the opioid on the B cells of the diabetic patients is specific for glucose. |
| 287 | 2951394 | Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. |
| 288 | 2951394 | To address the possibility that an abnormality in pancreatic beta-endorphin activity might contribute to abnormal insulin secretion in diabetes mellitus, we studied the effects of beta-endorphin infusion on islet function in diabetic patients. |
| 289 | 2951394 | The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. |
| 290 | 2951394 | Acute insulin and glucagon responses to arginine were not increased by beta-endorphin, suggesting that the effect of the opioid on the B cells of the diabetic patients is specific for glucose. |
| 291 | 2951394 | Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. |
| 292 | 2951394 | To address the possibility that an abnormality in pancreatic beta-endorphin activity might contribute to abnormal insulin secretion in diabetes mellitus, we studied the effects of beta-endorphin infusion on islet function in diabetic patients. |
| 293 | 2951394 | The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. |
| 294 | 2951394 | Acute insulin and glucagon responses to arginine were not increased by beta-endorphin, suggesting that the effect of the opioid on the B cells of the diabetic patients is specific for glucose. |
| 295 | 2951394 | Beta-endorphin infusion restores acute insulin responses to glucose in type-2 diabetes mellitus. |
| 296 | 2951394 | To address the possibility that an abnormality in pancreatic beta-endorphin activity might contribute to abnormal insulin secretion in diabetes mellitus, we studied the effects of beta-endorphin infusion on islet function in diabetic patients. |
| 297 | 2951394 | The iv infusion of human beta-endorphin at a dose of 0.5 mg/h for 2 h in type-2 non-insulin-dependent diabetic patients (n = 12) raised plasma insulin and glucagon levels and slightly but significantly lowered plasma glucose concentrations. beta-Endorphin infusion also resulted in reappearance of a clear-cut acute insulin response to glucose, while second phase insulin release was increased and glucose disposal accelerated. |
| 298 | 2951394 | Acute insulin and glucagon responses to arginine were not increased by beta-endorphin, suggesting that the effect of the opioid on the B cells of the diabetic patients is specific for glucose. |
| 299 | 2952536 | To determine the role of endogenous opiates in endotoxin-induced glucose-stimulated hyperinsulinism, plasma beta-endorphin, Met-enkephalin, Leu-enkephalin, insulin, and glucose concentrations were measured for 6 h in fasted, anesthetized dogs given LD70 of E. coli endotoxin; endotoxin and glucose; endotoxin, glucose, and naloxone (an opiate antagonist); glucose and naloxone; or glucose alone. |
| 300 | 2952536 | The elevation of plasma Met-enkephalin and beta-endorphin preceded the onset of hyperinsulinism, but the elevation of plasma Leu-enkephalin did not. |
| 301 | 2952536 | To determine the role of endogenous opiates in endotoxin-induced glucose-stimulated hyperinsulinism, plasma beta-endorphin, Met-enkephalin, Leu-enkephalin, insulin, and glucose concentrations were measured for 6 h in fasted, anesthetized dogs given LD70 of E. coli endotoxin; endotoxin and glucose; endotoxin, glucose, and naloxone (an opiate antagonist); glucose and naloxone; or glucose alone. |
| 302 | 2952536 | The elevation of plasma Met-enkephalin and beta-endorphin preceded the onset of hyperinsulinism, but the elevation of plasma Leu-enkephalin did not. |
| 303 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 304 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 305 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 306 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 307 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 308 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 309 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 310 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 311 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 312 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 313 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 314 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 315 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 316 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 317 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 318 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 319 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 320 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 321 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 322 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 323 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 324 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 325 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 326 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 327 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 328 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 329 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 330 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 331 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 332 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 333 | 2952663 | Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus. |
| 334 | 2952663 | The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. |
| 335 | 2952663 | In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. |
| 336 | 2952663 | In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. |
| 337 | 2952663 | There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. |
| 338 | 2952663 | The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. |
| 339 | 2958980 | GH, LH and cortisol responsiveness to combined im injection of TRH (10 micrograms/kg), GnRH (10 micrograms/kg), and ACTH (5 micrograms/kg) was determined in 9 MPA-treated and 9 control bitches at 17 months of treatment (Exp. |
| 340 | 2962893 | In normal dogs, beta endorphin diminished the insulin response to the first epinephrine infusion (p less than 0.02), and abolished this response to the second (p less than 0.05). |
| 341 | 2962893 | Also, beta endorphin failed to inhibit glucagon or insulin secretion in response to epinephrine in the diabetic animals. |
| 342 | 2962893 | In normal dogs, beta endorphin diminished the insulin response to the first epinephrine infusion (p less than 0.02), and abolished this response to the second (p less than 0.05). |
| 343 | 2962893 | Also, beta endorphin failed to inhibit glucagon or insulin secretion in response to epinephrine in the diabetic animals. |
| 344 | 2970411 | Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. |
| 345 | 2970411 | Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). |
| 346 | 2970411 | This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. |
| 347 | 2970411 | After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. |
| 348 | 2970411 | Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01). |
| 349 | 2970411 | Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. |
| 350 | 2970411 | Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). |
| 351 | 2970411 | This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. |
| 352 | 2970411 | After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. |
| 353 | 2970411 | Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01). |
| 354 | 2970411 | Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. |
| 355 | 2970411 | Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). |
| 356 | 2970411 | This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. |
| 357 | 2970411 | After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. |
| 358 | 2970411 | Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01). |
| 359 | 2970411 | Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. |
| 360 | 2970411 | Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). |
| 361 | 2970411 | This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. |
| 362 | 2970411 | After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. |
| 363 | 2970411 | Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01). |
| 364 | 2970411 | Beta-endorphin-induced inhibition and stimulation of insulin secretion in normal humans is glucose dependent. |
| 365 | 2970411 | Acute insulin and C-peptide responses to intravenous pulses of different glucose amounts (0.33 g/kg and 5 g) and arginine (3 g) were significantly reduced by beta-endorphin infusion (P less than .01). |
| 366 | 2970411 | This effect was associated with a significant reduction of the glucose disappearance rates, suggesting that the inhibition of insulin was of biological relevance. beta-Endorphin also inhibited glucose suppression of glucagon levels and augmented the glucagon response to arginine. |
| 367 | 2970411 | After stabilization of plasma glucose levels (350 +/- 34 mg/dl, t = 120 min), beta-endorphin infusion caused an immediate and marked increase in plasma insulin level (peak response 61 +/- 9 microU/ml, P less than .01), which remained elevated even after the discontinuation of opioid infusion. |
| 368 | 2970411 | Moreover, the acute insulin response to a glucose pulse (0.33 g/kg i.v.) given during beta-endorphin infusion during hyperglycemia was significantly higher than the response obtained during euglycemia (171 +/- 32 vs. 41 +/- 7 microU/ml, P less than .01). |
| 369 | 2973334 | [Behavior of beta-endorphin, GH, cortisol and glucagon during insulin hypoglycemia in type II diabetes]. |
| 370 | 2982980 | To assess in detail the adrenal function in this disorder, the responses of plasma aldosterone (PA) and its precursor steroids to angiotensin II (AII) infusion and adrenocorticotropic hormone (ACTH) injection were studied in seven patients with asymptomatic normoreninemic hypoaldosteronism (ANH) and 11 age-matched normal subjects. |
| 371 | 2986724 | The inhibitory effect of insulin was also observed in the release of S-100 protein induced by isoproterenol or adrenocorticotropin (ACTH), but not in the release induced by a high concentration (5 mM) of dibutyryl cyclic AMP. |
| 372 | 2986724 | The S-100 protein release induced by catecholamine was significantly decreased (to about 50%) in the fat pads obtained from insulin-injected rats. |
| 373 | 2986724 | These results suggest that the S-100 protein content in adipocytes is regulated by insulin as well as the lipolytic hormones. |
| 374 | 2991796 | Insulin therapy via minipump for 2 weeks did not alter this finding of lowered beta-endorphin concentrations in diabetic animals, despite normalization of blood glucose levels and body weight gain. |
| 375 | 2998913 | B-endorphin diminished the insulin and glucagon responses during the first epinephrine infusion and abolished them during the second, but did not alter the FFA, ACTH, or cortisol responses to epinephrine. |
| 376 | 3000117 | Effect of aging on growth hormone, ACTH and cortisol response to insulin-induced hypoglycemia in type I diabetes. |
| 377 | 3000117 | ACTH and cortisol responses to insulin were slightly decreased in the older diabetics. |
| 378 | 3000117 | Effect of aging on growth hormone, ACTH and cortisol response to insulin-induced hypoglycemia in type I diabetes. |
| 379 | 3000117 | ACTH and cortisol responses to insulin were slightly decreased in the older diabetics. |
| 380 | 3000733 | Effects of angiotensin II, adrenocorticotropin, and potassium on aldosterone production in adrenal zona glomerulosa cells from streptozotocin-induced diabetic rats. |
| 381 | 3000733 | To test the nature of the aldosterone deficiency, we investigated the responses of aldosterone production to angiotensin II (AII), ACTH, and potassium in adrenal zona glomerulosa cells from diabetic rats at 6 weeks after an injection of streptozotocin compared with those in the cells from control rats. |
| 382 | 3000733 | Effects of angiotensin II, adrenocorticotropin, and potassium on aldosterone production in adrenal zona glomerulosa cells from streptozotocin-induced diabetic rats. |
| 383 | 3000733 | To test the nature of the aldosterone deficiency, we investigated the responses of aldosterone production to angiotensin II (AII), ACTH, and potassium in adrenal zona glomerulosa cells from diabetic rats at 6 weeks after an injection of streptozotocin compared with those in the cells from control rats. |
| 384 | 3004244 | Tumor cells were focally immunoreactive for insulin, glucagon, and somatostatin and diffusely immunoreactive for alpha 1-antitrypsin as assayed by the avidin--biotin technique. |
| 385 | 3004244 | The tumor was immunonegative for human chorionic gonadotropin, gastrin, adrenocorticotropic hormone, and serotonin. |
| 386 | 3005748 | [Interaction of adrenocorticotropic hormone, cortisol and insulin during emotional tension among ischemic heart disease patients]. |
| 387 | 3005748 | Blood levels of the adenocorticotrophic hormone (ACTH), cortisol and insulin were measured in normal subjects and patients with different forms of coronary heart disease (CHD), aged 35 to 60 years and showing no signs of diabetes mellitus, obesity and arterial hypertension, under simulated emotional stress. |
| 388 | 3005748 | The majority of the patients, particularly those with unfavorable course of the CHD, showed stress-induced disturbances of hormonal control due to depressed insulin levels in the presence of an insignificant ACTH increment and high cortisolemia. |
| 389 | 3005748 | [Interaction of adrenocorticotropic hormone, cortisol and insulin during emotional tension among ischemic heart disease patients]. |
| 390 | 3005748 | Blood levels of the adenocorticotrophic hormone (ACTH), cortisol and insulin were measured in normal subjects and patients with different forms of coronary heart disease (CHD), aged 35 to 60 years and showing no signs of diabetes mellitus, obesity and arterial hypertension, under simulated emotional stress. |
| 391 | 3005748 | The majority of the patients, particularly those with unfavorable course of the CHD, showed stress-induced disturbances of hormonal control due to depressed insulin levels in the presence of an insignificant ACTH increment and high cortisolemia. |
| 392 | 3005748 | [Interaction of adrenocorticotropic hormone, cortisol and insulin during emotional tension among ischemic heart disease patients]. |
| 393 | 3005748 | Blood levels of the adenocorticotrophic hormone (ACTH), cortisol and insulin were measured in normal subjects and patients with different forms of coronary heart disease (CHD), aged 35 to 60 years and showing no signs of diabetes mellitus, obesity and arterial hypertension, under simulated emotional stress. |
| 394 | 3005748 | The majority of the patients, particularly those with unfavorable course of the CHD, showed stress-induced disturbances of hormonal control due to depressed insulin levels in the presence of an insignificant ACTH increment and high cortisolemia. |
| 395 | 3011344 | Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 396 | 3011344 | Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. |
| 397 | 3011344 | Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. |
| 398 | 3011344 | These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency. |
| 399 | 3011344 | Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 400 | 3011344 | Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. |
| 401 | 3011344 | Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. |
| 402 | 3011344 | These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency. |
| 403 | 3011344 | Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 404 | 3011344 | Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. |
| 405 | 3011344 | Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. |
| 406 | 3011344 | These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency. |
| 407 | 3032819 | In the present investigations, these animals have been studied in relation to the influence of low- and high-energy diets on body weight, plasma insulin and blood glucose levels, and on insulin secretion from the perfused pancreas and the secretion of corticotropin-like intermediate lobe peptide (CLIP, ACTH18-39) and the insulin secretagogue beta-cell-tropin (beta-CT, ACTH22-39) from the pituitary neurointermediate lobe. |
| 408 | 3034474 | Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 409 | 3034474 | Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. |
| 410 | 3034474 | These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency. |
| 411 | 3034474 | Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 412 | 3034474 | Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. |
| 413 | 3034474 | These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency. |
| 414 | 3034474 | Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. |
| 415 | 3034474 | Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. |
| 416 | 3034474 | These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency. |
| 417 | 3034756 | In the course of one-day normalization of glycemia by means of Biostator the TSH and prolactin rhythm was maintained, whereas the circadian rhythm of growth hormone and ACTH levels appeared with acrophase at 18.47 and 19.59 hour, respectively. |
| 418 | 3309934 | A study was made of the levels of glucose, IRI, STH, ACTH and cortisol in the blood serum (plasma) of 39 patients with diabetes mellitus prior to and after physical exercise testing. 25 patients performed physical exercises on an empty stomach in the morning (8-9 a.m.) 14 patients in the daytime (4-5 p.m.). |
| 419 | 3501746 | Impaired pancreatic polypeptide response to hCRF in type 2 diabetics: restoration to normal by an opioid antagonist. |
| 420 | 3501746 | Administration of synthetic human corticotropin-releasing factor (hCRF, 2 micrograms/kg body weight) to 6 normal men produced a significant rise in plasma pancreatic polypeptide (PP) levels. |
| 421 | 3510138 | Treatment with trypsin and carboxy-peptidase-B of high-molecular-weight peptides extracted from pancreas or islets resulted in release of additional met-enkephalin immunoreactivity, which was 39-fold enriched in islets compared with pancreas (5.90 +/- 0.58 and 0.153 +/- 0.032 pmol/mg protein, respectively). |
| 422 | 3514650 | A pituitary tumor was diagnosed in a prepubertal 13-yr-old girl, who had elevated plasma LH (58 mIU/ml) and PRL (93 ng/ml) levels; decreased GH, ACTH, and FSH secretion; and diabetes insipidus. |
| 423 | 3547015 | The administration of the long-acting met-enkephalin analogue (FK 33-824, Sandoz; Basel Switzerland) inhibits insulin secretion induced by glucose (oral and intravenous) and nonglucose (arginine and breakfast) secretagogues in both normal subjects and in patients with noninsulin-dependent diabetes mellitus. |
| 424 | 3877029 | We describe a male infant with septo-optic dysplasia in whom extensive endocrine evaluation revealed central diabetes insipidus, hypothalamic hypothyroidism and combined (hypothalamic-pituitary) hypoadrenalism, along with normal pituitary growth hormone reserve. |
| 425 | 3877029 | This is the first reported case of a patient with septo-optic dysplasia who underwent corticotropin-releasing factor and growth hormone-releasing hormone stimulation. |
| 426 | 3936737 | Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. |
| 427 | 3963792 | Hormones such as ACTH, STH, hydrocortisone, immunoreactive insulin and S-peptide, lipid metabolism and glycosylated hemoglobin were investigated in the time course of the treatment. |
| 428 | 4043329 | Antidiuretic hormone involvement in the release of alpha-melanocyte-stimulating hormone by hyperosmotic stimuli. |
| 429 | 4043329 | No such rise in alpha-MSH followed hypertonic saline administration in the Brattleboro (hereditary diabetes insipidus) animal (compared to isotonic saline injected controls). |
| 430 | 4043329 | Antidiuretic hormone involvement in the release of alpha-melanocyte-stimulating hormone by hyperosmotic stimuli. |
| 431 | 4043329 | No such rise in alpha-MSH followed hypertonic saline administration in the Brattleboro (hereditary diabetes insipidus) animal (compared to isotonic saline injected controls). |
| 432 | 4374289 | Luteinizing hormone, follicle-stimulating hormone, ACTH, and prolactin were not affected. |
| 433 | 6094152 | Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats. |
| 434 | 6094152 | To investigate alterations in aldosterone secretion in diabetes mellitus, the effects of angiotensin II, ACTH, and potassium on aldosterone secretion were examined in conscious unrestrained streptozotocin-induced diabetic rats (60 mg/kg, 12 weeks before study). |
| 435 | 6094152 | In chronic experimental diabetic rats where PRA, plasma aldosterone concentration, and urinary excretion of prostaglandin E2 were significantly decreased, a significant attenuated response of aldosterone secretion was demonstrated after infusion of angiotensin II, ACTH, or potassium. |
| 436 | 6094152 | Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats. |
| 437 | 6094152 | To investigate alterations in aldosterone secretion in diabetes mellitus, the effects of angiotensin II, ACTH, and potassium on aldosterone secretion were examined in conscious unrestrained streptozotocin-induced diabetic rats (60 mg/kg, 12 weeks before study). |
| 438 | 6094152 | In chronic experimental diabetic rats where PRA, plasma aldosterone concentration, and urinary excretion of prostaglandin E2 were significantly decreased, a significant attenuated response of aldosterone secretion was demonstrated after infusion of angiotensin II, ACTH, or potassium. |
| 439 | 6094152 | Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats. |
| 440 | 6094152 | To investigate alterations in aldosterone secretion in diabetes mellitus, the effects of angiotensin II, ACTH, and potassium on aldosterone secretion were examined in conscious unrestrained streptozotocin-induced diabetic rats (60 mg/kg, 12 weeks before study). |
| 441 | 6094152 | In chronic experimental diabetic rats where PRA, plasma aldosterone concentration, and urinary excretion of prostaglandin E2 were significantly decreased, a significant attenuated response of aldosterone secretion was demonstrated after infusion of angiotensin II, ACTH, or potassium. |
| 442 | 6243555 | No significant changes in plasma ACTH were observed in rats with coagulated hypophysial portal vessels or in Brattleboro rats with congenital diabetes insipidus. |
| 443 | 6252496 | Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro. |
| 444 | 6252496 | In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). |
| 445 | 6252496 | Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro. |
| 446 | 6252496 | In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). |
| 447 | 6257005 | Deficiencies of corticotrophin (ACTH), growth hormone, and prolactin were documented in a woman with diabetes mellitus and Sheehan's syndrome. |
| 448 | 6257005 | The patient's ACTH deficit appeared to be secondary to a hypothalamic abnormality since on two occasions the patient had a marked plasma ACTH response to vasopressin but not to insulin induced hypoglycaemia. |
| 449 | 6257005 | Deficiencies of corticotrophin (ACTH), growth hormone, and prolactin were documented in a woman with diabetes mellitus and Sheehan's syndrome. |
| 450 | 6257005 | The patient's ACTH deficit appeared to be secondary to a hypothalamic abnormality since on two occasions the patient had a marked plasma ACTH response to vasopressin but not to insulin induced hypoglycaemia. |
| 451 | 6258694 | 1 beta-Endorphin (2 micrograms injected into the lateral ventricles) produced a significant decrease in the urine outflow and in the excretion of Na+ and K+ in Brattleboro rats, animals suffering from severe diabetes insipidus. |
| 452 | 6269688 | To investigate this possibility the plasma met-enkephalin and beta-endorphin responses to sherry with and without chlorpropamide were studied in six patients with non-insulin dependent diabetes and in six normal subjects. |
| 453 | 6277121 | ACTH values at 08(00) and 18(00), hPRL and TSh secretion in response to 200 microgram TRH i.v., and GH secretion in response to 500 mg oral L-dopa were evaluated. |
| 454 | 6281608 | Baseline endocrine studies (serum triglycerides: 2600 mg/dl) demonstrated hyperprolactinemia (serum prolactin 51 ng/ml), increased ACTH levels, absence of suppression of ACTH to a high dose of dexamethasone which suppressed serum cortisol normally and, hyperresponsiveness of TSH to stimulation with TRH. |
| 455 | 6281608 | Repeat endocrine function studies (serum triglycerides: 700 mg/dl) showed a further rise in serum prolactin (greater than 160 ng/ml), persistence of abnormal ACTH secretion and normalization of TSH responsiveness. |
| 456 | 6281608 | Baseline endocrine studies (serum triglycerides: 2600 mg/dl) demonstrated hyperprolactinemia (serum prolactin 51 ng/ml), increased ACTH levels, absence of suppression of ACTH to a high dose of dexamethasone which suppressed serum cortisol normally and, hyperresponsiveness of TSH to stimulation with TRH. |
| 457 | 6281608 | Repeat endocrine function studies (serum triglycerides: 700 mg/dl) showed a further rise in serum prolactin (greater than 160 ng/ml), persistence of abnormal ACTH secretion and normalization of TSH responsiveness. |
| 458 | 6288750 | Corticotropin-releasing factor (CRF) was administered as an iv bolus to two young women with mild Cushing's disease shortly before and one week after successful transsphenoidal microadenomectomy. |
| 459 | 6288750 | The dose of CRF (1 microgram/kg body weight) had previously been shown to stimulate increased plasma ACTH and cortisol in normal subjects. |
| 460 | 6288750 | After surgery, at a time when plasma cortisol was maintained at similar levels with exogenous hydrocortisone, there was no plasma ACTH or LH, TSH and prolactin increased after administration of LRH and TRH, and GH increased in response to insulin-induced hypoglycemia. |
| 461 | 6288750 | CRF-induced increments in ACTH and cortisol were much less, but the time course was similar and peak levels attained were still higher than those in normal subjects. |
| 462 | 6288750 | Corticotropin-releasing factor (CRF) was administered as an iv bolus to two young women with mild Cushing's disease shortly before and one week after successful transsphenoidal microadenomectomy. |
| 463 | 6288750 | The dose of CRF (1 microgram/kg body weight) had previously been shown to stimulate increased plasma ACTH and cortisol in normal subjects. |
| 464 | 6288750 | After surgery, at a time when plasma cortisol was maintained at similar levels with exogenous hydrocortisone, there was no plasma ACTH or LH, TSH and prolactin increased after administration of LRH and TRH, and GH increased in response to insulin-induced hypoglycemia. |
| 465 | 6288750 | CRF-induced increments in ACTH and cortisol were much less, but the time course was similar and peak levels attained were still higher than those in normal subjects. |
| 466 | 6288750 | Corticotropin-releasing factor (CRF) was administered as an iv bolus to two young women with mild Cushing's disease shortly before and one week after successful transsphenoidal microadenomectomy. |
| 467 | 6288750 | The dose of CRF (1 microgram/kg body weight) had previously been shown to stimulate increased plasma ACTH and cortisol in normal subjects. |
| 468 | 6288750 | After surgery, at a time when plasma cortisol was maintained at similar levels with exogenous hydrocortisone, there was no plasma ACTH or LH, TSH and prolactin increased after administration of LRH and TRH, and GH increased in response to insulin-induced hypoglycemia. |
| 469 | 6288750 | CRF-induced increments in ACTH and cortisol were much less, but the time course was similar and peak levels attained were still higher than those in normal subjects. |
| 470 | 6288750 | Corticotropin-releasing factor (CRF) was administered as an iv bolus to two young women with mild Cushing's disease shortly before and one week after successful transsphenoidal microadenomectomy. |
| 471 | 6288750 | The dose of CRF (1 microgram/kg body weight) had previously been shown to stimulate increased plasma ACTH and cortisol in normal subjects. |
| 472 | 6288750 | After surgery, at a time when plasma cortisol was maintained at similar levels with exogenous hydrocortisone, there was no plasma ACTH or LH, TSH and prolactin increased after administration of LRH and TRH, and GH increased in response to insulin-induced hypoglycemia. |
| 473 | 6288750 | CRF-induced increments in ACTH and cortisol were much less, but the time course was similar and peak levels attained were still higher than those in normal subjects. |
| 474 | 6293899 | Responsiveness of plasma 18-hydroxycorticosterone and aldosterone to angiotensin II or corticotropin in nonazotemic diabetes mellitus. |
| 475 | 6295233 | Molecular forms and anterior pituitary content of ACTH, beta-lipotropin, and beta-endorphin in diabetes insipidus di/di (Brattleboro) rats. |
| 476 | 6296674 | To evaluate this possibility, we infused synthetic human beta-endorphin intravenously in healthy volunteers and in insulin-dependent diabetic patients. |
| 477 | 6296674 | In nondiabetic subjects, beta-endorphin also increased plasma insulin concentrations. |
| 478 | 6296674 | Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. |
| 479 | 6296674 | To evaluate this possibility, we infused synthetic human beta-endorphin intravenously in healthy volunteers and in insulin-dependent diabetic patients. |
| 480 | 6296674 | In nondiabetic subjects, beta-endorphin also increased plasma insulin concentrations. |
| 481 | 6296674 | Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. |
| 482 | 6296674 | To evaluate this possibility, we infused synthetic human beta-endorphin intravenously in healthy volunteers and in insulin-dependent diabetic patients. |
| 483 | 6296674 | In nondiabetic subjects, beta-endorphin also increased plasma insulin concentrations. |
| 484 | 6296674 | Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. |
| 485 | 6299123 | To study the role of the paraventricular nucleus and of neurohypophysial hormones in the control of ACTH secretion, the paraventricular nuclei (PV) of Brattleboro diabetes insipidus rats (DI) were lesioned (L) with a knife; sham-lesioned DI (S) served as controls. |
| 486 | 6299123 | The median eminence (ME) and neural lobe (NL) were homogenized in 50 microliters of 0.1 N HCl and frozen pending bioassay of corticotropin-releasing factor (CRF). |
| 487 | 6299123 | To study the role of the paraventricular nucleus and of neurohypophysial hormones in the control of ACTH secretion, the paraventricular nuclei (PV) of Brattleboro diabetes insipidus rats (DI) were lesioned (L) with a knife; sham-lesioned DI (S) served as controls. |
| 488 | 6299123 | The median eminence (ME) and neural lobe (NL) were homogenized in 50 microliters of 0.1 N HCl and frozen pending bioassay of corticotropin-releasing factor (CRF). |
| 489 | 6300594 | Diabetic animals were found to have a marked increase in endorphin equivalents, measured by opiate receptor binding assay, in the NIL whereas no change was observed in beta endorphin-like immunoreactivity (beta ELI) or ACTH measured by RIA. |
| 490 | 6318561 | In the pregnant patients with fetuses affected by Cooley's disease (second trimester) and in those with edema-proteinuria-hypertension (EPH) gestosis (third trimester), amniotic fluid levels of beta-endorphin, beta-lipotropin, and ACTH were in the same range as those in healthy pregnant women. |
| 491 | 6319955 | Beta-endorphin stimulates the secretion of insulin and glucagon in diabetes mellitus. |
| 492 | 6319955 | Administration of human beta-endorphin (2.5 mg IV bolus) to three subjects with non-insulin-dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes. |
| 493 | 6319955 | Beta-endorphin stimulates the secretion of insulin and glucagon in diabetes mellitus. |
| 494 | 6319955 | Administration of human beta-endorphin (2.5 mg IV bolus) to three subjects with non-insulin-dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes. |
| 495 | 6488662 | One of the patients demonstrated adrenocorticotropic hormone deficiency, and one had diabetes insipidus. |
| 496 | 6499230 | The response of plasma immunoreactive met-enkephalin (IR-met-enkephalin) to ethanol (8 g by mouth) after chlorpropamide (250 mg daily for 14 d) was studied in three groups of non-insulin dependent diabetics (a) six diabetics who showed chlorpropamide alcohol flush (CPAF) and in whom the reaction could be blocked by indomethacin, (b) five diabetics who showed CPAF but in whom the flush could not be blocked by indomethacin and (c) five diabetics who did not show CPAF. |
| 497 | 6534872 | Release of alpha-MSH from the in vitro superfused neuro-intermediate lobe of the pituitary of the rat by antidiuretic hormone. |
| 498 | 6534872 | The effect of antidiuretic hormone (ADH) on the release of immunoreactive alpha-melanocyte stimulating hormone (alpha-MSH) from the superfused neurointermediate lobe of the pituitary of the normal Wistar and Brattleboro (diabetes insipidus) rat was studied in vitro. |
| 499 | 6534872 | Release of alpha-MSH from the in vitro superfused neuro-intermediate lobe of the pituitary of the rat by antidiuretic hormone. |
| 500 | 6534872 | The effect of antidiuretic hormone (ADH) on the release of immunoreactive alpha-melanocyte stimulating hormone (alpha-MSH) from the superfused neurointermediate lobe of the pituitary of the normal Wistar and Brattleboro (diabetes insipidus) rat was studied in vitro. |
| 501 | 6672071 | He was found to have marked hypothalamic-pituitary dysfunction including deficiencies of growth hormone, thyrotropin, adrenocorticotropic hormone and gonadotropins, diabetes insipidus, adipsia with essential hypernatremia and poikilothermia. |
| 502 | 6874170 | In addition to insulin deficiency and impaired catecholamine secretion, diabetics showed high values of growth hormone, ACTH, and cortisol. |
| 503 | 6983849 | Demonstration of corticotropin-releasing factor (CRF) activity in the neurohypophysis of Brattleboro rats. |
| 504 | 7007886 | We have compared the distribution of oxytocin, vasopressin and enkephalin immunoreactivity (IR) in the neurohypophysis of the rat, and report here that Met-enkephalin-IR is invariably associated with nerve terminals that contain oxytocin-IR whereas the terminals that contain vasopressin-IR often, but not invariably, are Leu-enkephalin immunoreactive. |
| 505 | 7418926 | ["Hormone receptor diseases" in Japan: A nation-wide survey for testicular feminization syndrome, pseudohypoparathyroidism, nephrogenic diabetes insipidus, Bartter's syndrome and congenital adrenocortical unresponsiveness to ACTH (author's transl)]. |
| 506 | 7418926 | The approximate numbers of patients in Japan estimated from these surveys are the following: testicular feminization syndrome (TFS), 390; pseudohypoparathyroidism (PHP), 220, nephrogenic diabetes insipidus (NDI), 280; Bartter's syndrome, 90; congenital adrenocortical unresponsiveness to ACTH (CAUA), 18. |
| 507 | 7418926 | ["Hormone receptor diseases" in Japan: A nation-wide survey for testicular feminization syndrome, pseudohypoparathyroidism, nephrogenic diabetes insipidus, Bartter's syndrome and congenital adrenocortical unresponsiveness to ACTH (author's transl)]. |
| 508 | 7418926 | The approximate numbers of patients in Japan estimated from these surveys are the following: testicular feminization syndrome (TFS), 390; pseudohypoparathyroidism (PHP), 220, nephrogenic diabetes insipidus (NDI), 280; Bartter's syndrome, 90; congenital adrenocortical unresponsiveness to ACTH (CAUA), 18. |
| 509 | 7479313 | NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action. |
| 510 | 7479313 | The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release. |
| 511 | 7479313 | The ARC-PVN projection appears to be overactive in insulin-deficient diabetic rats, and could contribute to the compensatory hyperphagia and reduced energy expenditure, and pituitary dysfunction found in these animals; overactivity of these NPY neurons may be due to reduction of insulin's normal inhibitory effect. |
| 512 | 7479313 | The ARC-PVN projection is also stimulated in rat models of obesity +/- non-insulin diabetes, possibly because the hypothalamus is resistant to inhibition by insulin; in these animals, enhanced activity of ARC NPY neurons could cause hyperphagia, reduced energy expenditure, and obesity, and perhaps contribute to hyperinsulinemia and altered pituitary secretion. |
| 513 | 7494779 | Like any other pancreatic islet cell carcinoma, a somatostatinoma may also produce several different hormones such as adrenocorticotropic hormone, calcitonin, vasoactive intestinal polypeptide, pancreatic polypeptide, gastrin, insulin, and glucagon. |
| 514 | 7494779 | We present a patient with somatostatinoma in which an immunocytochemical study of the specimens from pancreas and liver showed a weak positive reaction for gastrin besides a strong positive reaction for somatostatin. |
| 515 | 7535623 | Serum gamma-globulins from patients 1 and 4 attenuated corticotropin releasing hormone-induced ACTH release in monolayer cultured rat anterior pituitary cells. |
| 516 | 7584524 | Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, clonidine, and moxonidine concentrations. |
| 517 | 7584534 | In the five patients submitted to inferior petrosal sinus sampling, a parallelism between ACTH and PRL concentrations could be observed with a PRL rise, ipsilateral to that of ACTH, ensuing in three patients after administration of corticotropin-releasing hormone. |
| 518 | 7619655 | The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. |
| 519 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 520 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 521 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 522 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 523 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 524 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 525 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 526 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 527 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 528 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 529 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 530 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 531 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 532 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 533 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 534 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 535 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 536 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 537 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 538 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 539 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 540 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 541 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 542 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 543 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 544 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 545 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 546 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 547 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 548 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 549 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 550 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 551 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 552 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 553 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 554 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 555 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 556 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 557 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 558 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 559 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 560 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 561 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 562 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 563 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 564 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 565 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 566 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 567 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 568 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 569 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 570 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 571 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 572 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 573 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 574 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 575 | 7659194 | Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. |
| 576 | 7659194 | In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. |
| 577 | 7659194 | The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. |
| 578 | 7659194 | We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. |
| 579 | 7659194 | Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. |
| 580 | 7659194 | In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. |
| 581 | 7659194 | The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. |
| 582 | 7659194 | We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion. |
| 583 | 7683121 | Assessment of hypothalamic-pituitary function before treatment revealed pituitary deficits in all patients involving growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and adrenocorticotropic hormone. |
| 584 | 7712683 | Therefore, in our study naloxone infusion seems to have beta-endorphin-like effects in non-diabetic obese subjects by increasing their glycemic levels, with no evidence of expected insulin decrease. |
| 585 | 7714765 | Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. |
| 586 | 7714765 | Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. |
| 587 | 7714765 | Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. |
| 588 | 7714765 | Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. |
| 589 | 7723679 | Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. |
| 590 | 7723679 | Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. |
| 591 | 7723679 | When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). |
| 592 | 7723679 | Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. |
| 593 | 7723679 | Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. |
| 594 | 7723679 | When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). |
| 595 | 7723679 | Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. |
| 596 | 7723679 | Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. |
| 597 | 7723679 | When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). |
| 598 | 7757071 | As predicted by the interactions of mouse agouti with the extension gene (which encodes the melanocyte receptor for alpha-melanocyte stimulating hormone [alpha-MSH]), expression of ASP in transgenic mice produces a yellow coat, and expression of ASP in cell culture blocks the alpha-MSH-stimulated accumulation of cAMP in mouse melanoma cells. |
| 599 | 7757071 | The localization of ASP relative to other loci on chromosome 20 excludes it as a candidate for the MODY1 locus, a gene responsible for one form of early-onset non-insulin-dependent diabetes mellitus or maturity-onset diabetes of the young. |
| 600 | 7784456 | Neither basal ACTH secretion nor the ACTH response to corticotropin-releasing hormone (CRH) was affected by pathophysiological molar ratios of FFA:BSA. |
| 601 | 7801492 | Diabetes insipidus in a dog with an alpha MSH-producing pituitary tumor. |
| 602 | 7821733 | This resulted in an insulin resistance of all muscle types that was due to an increased glucose-fatty acid cycle, without measurable alteration of the GLUT 4 system. |
| 603 | 7821733 | This could be the reason for adaptive changes leading to increased levels in their hypothalamic neuropeptide Y levels and median eminence corticotropin-releasing-factor. |
| 604 | 7854093 | The laboratory findings showed deficiency of cortocotropin (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and slight hyperprolactinemia (PRL). |
| 605 | 7903584 | Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. |
| 606 | 7903584 | Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 607 | 7903584 | CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. |
| 608 | 7903584 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process. |
| 609 | 7903584 | Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. |
| 610 | 7903584 | Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 611 | 7903584 | CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. |
| 612 | 7903584 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process. |
| 613 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 614 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 615 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 616 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 617 | 7904782 | Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. |
| 618 | 7904782 | Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. |
| 619 | 7904782 | CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. |
| 620 | 7904782 | Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process. |
| 621 | 7938053 | The studies reported herein were conducted to confirm that the pituitary gland is involved in maintaining growth hormone (GH) resistance in rats with insulin-dependent diabetes mellitus (IDDM) and to determine whether the adrenocorticotropic hormone (ACTH)-adrenal cortical axis is responsible. |
| 622 | 7938053 | These studies confirm that the pituitary contributes to diabetic growth impairment and show that the ACTH-adrenal cortical axis is primarily responsible for the GH-resistant state that develops in rats with IDDM. |
| 623 | 7938053 | The studies reported herein were conducted to confirm that the pituitary gland is involved in maintaining growth hormone (GH) resistance in rats with insulin-dependent diabetes mellitus (IDDM) and to determine whether the adrenocorticotropic hormone (ACTH)-adrenal cortical axis is responsible. |
| 624 | 7938053 | These studies confirm that the pituitary contributes to diabetic growth impairment and show that the ACTH-adrenal cortical axis is primarily responsible for the GH-resistant state that develops in rats with IDDM. |
| 625 | 7951540 | Low plasma corticotropin-releasing hormone (CRH) levels in patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 626 | 7951540 | Plasma CRH levels were measured in patients with non-insulin dependent diabetes mellitus (NIDDM) as the pituitary-adrenal abnormalities have been reported in NIDDM. |
| 627 | 7951540 | They were also measured after oral administration of 75 g glucose to examine whether glucose increased plasma CRH along with insulin secretion. |
| 628 | 7951540 | Plasma CRH, ACTH and cortisol did not change after glucose administration in either NIDDM patients or controls. |
| 629 | 7951540 | Neither plasma CRH nor ACTH showed a significant correlation with plasma glucose or insulin response in NIDDM patients. |
| 630 | 7951540 | These results suggest that CRH secretion is not stimulated by glucose, that plasma ACTH and cortisol are increased in NIDDM patients and that CRH is not responsible for these increases. |
| 631 | 7951540 | Low plasma corticotropin-releasing hormone (CRH) levels in patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 632 | 7951540 | Plasma CRH levels were measured in patients with non-insulin dependent diabetes mellitus (NIDDM) as the pituitary-adrenal abnormalities have been reported in NIDDM. |
| 633 | 7951540 | They were also measured after oral administration of 75 g glucose to examine whether glucose increased plasma CRH along with insulin secretion. |
| 634 | 7951540 | Plasma CRH, ACTH and cortisol did not change after glucose administration in either NIDDM patients or controls. |
| 635 | 7951540 | Neither plasma CRH nor ACTH showed a significant correlation with plasma glucose or insulin response in NIDDM patients. |
| 636 | 7951540 | These results suggest that CRH secretion is not stimulated by glucose, that plasma ACTH and cortisol are increased in NIDDM patients and that CRH is not responsible for these increases. |
| 637 | 7951540 | Low plasma corticotropin-releasing hormone (CRH) levels in patients with non-insulin dependent diabetes mellitus (NIDDM). |
| 638 | 7951540 | Plasma CRH levels were measured in patients with non-insulin dependent diabetes mellitus (NIDDM) as the pituitary-adrenal abnormalities have been reported in NIDDM. |
| 639 | 7951540 | They were also measured after oral administration of 75 g glucose to examine whether glucose increased plasma CRH along with insulin secretion. |
| 640 | 7951540 | Plasma CRH, ACTH and cortisol did not change after glucose administration in either NIDDM patients or controls. |
| 641 | 7951540 | Neither plasma CRH nor ACTH showed a significant correlation with plasma glucose or insulin response in NIDDM patients. |
| 642 | 7951540 | These results suggest that CRH secretion is not stimulated by glucose, that plasma ACTH and cortisol are increased in NIDDM patients and that CRH is not responsible for these increases. |
| 643 | 7956715 | The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. |
| 644 | 7956715 | All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). |
| 645 | 7956715 | These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. |
| 646 | 7956715 | The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. |
| 647 | 7956715 | All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). |
| 648 | 7956715 | These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. |
| 649 | 7956715 | The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. |
| 650 | 7956715 | All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). |
| 651 | 7956715 | These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. |
| 652 | 7957502 | Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). |
| 653 | 7957502 | In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. |
| 654 | 7957502 | The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. |
| 655 | 7957502 | Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). |
| 656 | 7957502 | In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. |
| 657 | 7957502 | The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. |
| 658 | 7957502 | Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). |
| 659 | 7957502 | In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. |
| 660 | 7957502 | The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. |
| 661 | 7962332 | Counterregulatory hormone responses to hypoglycemia are impaired in subjects with insulin-dependent diabetes mellitus (IDDM) in strict glycemic control. |
| 662 | 7962332 | The ACTH response to hypoglycemia was not significantly reduced in the well controlled IDDM, whereas the response to metyrapone was actually greater in this group (P < 0.05 vs. poorly controlled IDDM). |
| 663 | 7962332 | These data suggest that 1) the reduced epinephrine responses in well controlled IDDM may not be specific for the hypoglycemic stimulus alone, but may also occur in response to other nonhypoglycemic stimuli; 2) cortisol responses to hypoglycemia are reduced in well controlled IDDM, whereas the ACTH response to a non-hypoglycemic stimulus remains intact; and 3) GH responses to both hypoglycemic and nonhypoglycemic stimuli are preserved in well controlled IDDM. |
| 664 | 7962332 | The preservation of ACTH and GH responses to metyrapone and arginine, respectively, suggests adequate pituitary functional reserve in IDDM patients in strict glycemic control in response to nonhypoglycemic stimuli. |
| 665 | 7962332 | Counterregulatory hormone responses to hypoglycemia are impaired in subjects with insulin-dependent diabetes mellitus (IDDM) in strict glycemic control. |
| 666 | 7962332 | The ACTH response to hypoglycemia was not significantly reduced in the well controlled IDDM, whereas the response to metyrapone was actually greater in this group (P < 0.05 vs. poorly controlled IDDM). |
| 667 | 7962332 | These data suggest that 1) the reduced epinephrine responses in well controlled IDDM may not be specific for the hypoglycemic stimulus alone, but may also occur in response to other nonhypoglycemic stimuli; 2) cortisol responses to hypoglycemia are reduced in well controlled IDDM, whereas the ACTH response to a non-hypoglycemic stimulus remains intact; and 3) GH responses to both hypoglycemic and nonhypoglycemic stimuli are preserved in well controlled IDDM. |
| 668 | 7962332 | The preservation of ACTH and GH responses to metyrapone and arginine, respectively, suggests adequate pituitary functional reserve in IDDM patients in strict glycemic control in response to nonhypoglycemic stimuli. |
| 669 | 7962332 | Counterregulatory hormone responses to hypoglycemia are impaired in subjects with insulin-dependent diabetes mellitus (IDDM) in strict glycemic control. |
| 670 | 7962332 | The ACTH response to hypoglycemia was not significantly reduced in the well controlled IDDM, whereas the response to metyrapone was actually greater in this group (P < 0.05 vs. poorly controlled IDDM). |
| 671 | 7962332 | These data suggest that 1) the reduced epinephrine responses in well controlled IDDM may not be specific for the hypoglycemic stimulus alone, but may also occur in response to other nonhypoglycemic stimuli; 2) cortisol responses to hypoglycemia are reduced in well controlled IDDM, whereas the ACTH response to a non-hypoglycemic stimulus remains intact; and 3) GH responses to both hypoglycemic and nonhypoglycemic stimuli are preserved in well controlled IDDM. |
| 672 | 7962332 | The preservation of ACTH and GH responses to metyrapone and arginine, respectively, suggests adequate pituitary functional reserve in IDDM patients in strict glycemic control in response to nonhypoglycemic stimuli. |
| 673 | 8045962 | Our data demonstrate the existence of a very early phase of Addison's disease in which adrenal function shows an impaired response to ovine CRH-stimulated ACTH. |
| 674 | 8070123 | The possible influence of both beta-endorphin and insulin secretion on diabetes development in pregnant women was studied by means of radioimmunoassay technique (RIA-Nichols Institute). |
| 675 | 8070123 | Beta endorphin increase was found in both groups, according to the progression of gestation, and the rise was significantly higher in the insulin-dependent group. |
| 676 | 8070123 | The possible influence of both beta-endorphin and insulin secretion on diabetes development in pregnant women was studied by means of radioimmunoassay technique (RIA-Nichols Institute). |
| 677 | 8070123 | Beta endorphin increase was found in both groups, according to the progression of gestation, and the rise was significantly higher in the insulin-dependent group. |
| 678 | 8117990 | Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. |
| 679 | 8117990 | Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. |
| 680 | 8117990 | Acute acidosis stimulates insulin and corticotropin secretions acute alkalosis reduces blood insulin and corticotropin levels and increases glucagon concentration. |
| 681 | 8117990 | Chronic acidosis and alkalosis decrease insulin secretion and stimulates corticotropin secretion. |
| 682 | 8130884 | It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. |
| 683 | 8130884 | With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 micrograms iv as a bolus) in 18 normal subjects (15 females and three males, age 22-35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16-40 years). |
| 684 | 8130884 | The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean +/- SEM: 17.0 +/- 1.2 vs 7.7 +/- 0.7 pmol/l, p = 0.0003; cortisol: 611.3 +/- 59.4 vs 450.7 +/- 21.2 nmol/l, p = 0.01) or area under curve values (ACTH: 672.5 +/- 75.7 vs 364.0 +/- 33.6 pmol.l-1 x h-1, p = 0.002; cortisol: 29158.0 +/- 2937.0 vs 23236.7 +/- 1052.1 nmol.l-1 x h-1, p = 0.03). |
| 685 | 8130884 | These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. |
| 686 | 8130884 | It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. |
| 687 | 8130884 | With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 micrograms iv as a bolus) in 18 normal subjects (15 females and three males, age 22-35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16-40 years). |
| 688 | 8130884 | The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean +/- SEM: 17.0 +/- 1.2 vs 7.7 +/- 0.7 pmol/l, p = 0.0003; cortisol: 611.3 +/- 59.4 vs 450.7 +/- 21.2 nmol/l, p = 0.01) or area under curve values (ACTH: 672.5 +/- 75.7 vs 364.0 +/- 33.6 pmol.l-1 x h-1, p = 0.002; cortisol: 29158.0 +/- 2937.0 vs 23236.7 +/- 1052.1 nmol.l-1 x h-1, p = 0.03). |
| 689 | 8130884 | These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. |
| 690 | 8130884 | It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. |
| 691 | 8130884 | With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 micrograms iv as a bolus) in 18 normal subjects (15 females and three males, age 22-35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16-40 years). |
| 692 | 8130884 | The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean +/- SEM: 17.0 +/- 1.2 vs 7.7 +/- 0.7 pmol/l, p = 0.0003; cortisol: 611.3 +/- 59.4 vs 450.7 +/- 21.2 nmol/l, p = 0.01) or area under curve values (ACTH: 672.5 +/- 75.7 vs 364.0 +/- 33.6 pmol.l-1 x h-1, p = 0.002; cortisol: 29158.0 +/- 2937.0 vs 23236.7 +/- 1052.1 nmol.l-1 x h-1, p = 0.03). |
| 693 | 8130884 | These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. |
| 694 | 8136620 | The release of different amounts of beta-endorphin, growth hormone, and adrenocorticotropin during human (HI) and porcine (PI) insulin-induced hypoglycemia would serve as a pointer to a different insulin species effect on hypothalamic-pituitary response. |
| 695 | 8136620 | The glucose clamp technique was used to lower the blood glucose concentration stepwise (3.3, 2.2, 1.7 mmol/l) over similar periods in ten patients with insulin-dependent diabetes mellitus. beta-endorphin, growth hormone, and adrenocorticotropin levels were determined by radioimmunoassay from arterialized blood at the above plateaus. |
| 696 | 8136620 | The release of different amounts of beta-endorphin, growth hormone, and adrenocorticotropin during human (HI) and porcine (PI) insulin-induced hypoglycemia would serve as a pointer to a different insulin species effect on hypothalamic-pituitary response. |
| 697 | 8136620 | The glucose clamp technique was used to lower the blood glucose concentration stepwise (3.3, 2.2, 1.7 mmol/l) over similar periods in ten patients with insulin-dependent diabetes mellitus. beta-endorphin, growth hormone, and adrenocorticotropin levels were determined by radioimmunoassay from arterialized blood at the above plateaus. |
| 698 | 8162147 | Endocrinological findings showed a decreased ACTH, gonadotropin and growth hormone more frequently while there were 2 cases of hyperprolactinemia and 1 case of diabetes insipidus. |
| 699 | 8173950 | Although some of the brain structures are known to express mRNA encoding a gamma-MSH-preferring melanocortin receptor type known as MC3, the relative order of binding affinities of melanocortins, determined in concentration-response studies, was NDP-MSH > or = ACTH1-24 > or = alpha-MSH > gamma-MSH > ACTH4-10 in all brain structures. |
| 700 | 8239172 | To investigate the activity of the endogenous opioid system in patients with insulin-dependent diabetes mellitus during ventilatory stress situations, we measured plasma beta-endorphin levels in six male and five female diabetic patients breathing against fatiguing inspiratory resistive loads. |
| 701 | 8243290 | Despite the observed facilitation of morning stress-induced ACTH secretion in STZ-diabetic rats, there were no differences in hypothalamic CRF content between control and STZ-diabetic tissue. |
| 702 | 8283258 | Fifteen (41.7%) had prolactin (PRL)-secreting tumors, 16 (44.4%) had adrenocorticotropic hormone (ACTH)-secreting tumors (including two patients with Nelson-Salassa syndrome), and three (8.3%) had tumors secreting growth hormone (GH); two patients (5.6%) had clinically nonfunctioning tumors. |
| 703 | 8283258 | Long-term follow-up review (median > 5 years) revealed good control of PRL-secreting tumors (although five of 15 patients had received postoperative radiotherapy), contrasted with a 25% late recurrence rate for ACTH-secreting tumors, which had an 80% initial remission rate. |
| 704 | 8283258 | It is concluded that: 1) although pediatric pituitary adenomas occur primarily in adolescence, Cushing's disease is found at any age; 2) transsphenoidal surgery is feasible and safe in this age group; 3) plurihormonal tumors occur more frequently in the pediatric age group than in adults; and 4) long-term control rates in PRL- and ACTH-secreting tumors are probably similar to those seen in adults. |
| 705 | 8283258 | Fifteen (41.7%) had prolactin (PRL)-secreting tumors, 16 (44.4%) had adrenocorticotropic hormone (ACTH)-secreting tumors (including two patients with Nelson-Salassa syndrome), and three (8.3%) had tumors secreting growth hormone (GH); two patients (5.6%) had clinically nonfunctioning tumors. |
| 706 | 8283258 | Long-term follow-up review (median > 5 years) revealed good control of PRL-secreting tumors (although five of 15 patients had received postoperative radiotherapy), contrasted with a 25% late recurrence rate for ACTH-secreting tumors, which had an 80% initial remission rate. |
| 707 | 8283258 | It is concluded that: 1) although pediatric pituitary adenomas occur primarily in adolescence, Cushing's disease is found at any age; 2) transsphenoidal surgery is feasible and safe in this age group; 3) plurihormonal tumors occur more frequently in the pediatric age group than in adults; and 4) long-term control rates in PRL- and ACTH-secreting tumors are probably similar to those seen in adults. |
| 708 | 8283258 | Fifteen (41.7%) had prolactin (PRL)-secreting tumors, 16 (44.4%) had adrenocorticotropic hormone (ACTH)-secreting tumors (including two patients with Nelson-Salassa syndrome), and three (8.3%) had tumors secreting growth hormone (GH); two patients (5.6%) had clinically nonfunctioning tumors. |
| 709 | 8283258 | Long-term follow-up review (median > 5 years) revealed good control of PRL-secreting tumors (although five of 15 patients had received postoperative radiotherapy), contrasted with a 25% late recurrence rate for ACTH-secreting tumors, which had an 80% initial remission rate. |
| 710 | 8283258 | It is concluded that: 1) although pediatric pituitary adenomas occur primarily in adolescence, Cushing's disease is found at any age; 2) transsphenoidal surgery is feasible and safe in this age group; 3) plurihormonal tumors occur more frequently in the pediatric age group than in adults; and 4) long-term control rates in PRL- and ACTH-secreting tumors are probably similar to those seen in adults. |
| 711 | 8294562 | Insulin does not appear to be involved in the expression of lymphocyte GH or POMC. |
| 712 | 8294562 | The administration of insulin to the diabetic animals had no significant effect on the expression of GH or POMC by the immune cells. |
| 713 | 8294562 | In addition, lymphocytes do not appear to serve as a source of insulin or are the expression of genes for lymphocyte GH or ACTH altered by insulin in vitro. |
| 714 | 8294562 | Insulin does not appear to be involved in the expression of lymphocyte GH or POMC. |
| 715 | 8294562 | The administration of insulin to the diabetic animals had no significant effect on the expression of GH or POMC by the immune cells. |
| 716 | 8294562 | In addition, lymphocytes do not appear to serve as a source of insulin or are the expression of genes for lymphocyte GH or ACTH altered by insulin in vitro. |
| 717 | 8294562 | Insulin does not appear to be involved in the expression of lymphocyte GH or POMC. |
| 718 | 8294562 | The administration of insulin to the diabetic animals had no significant effect on the expression of GH or POMC by the immune cells. |
| 719 | 8294562 | In addition, lymphocytes do not appear to serve as a source of insulin or are the expression of genes for lymphocyte GH or ACTH altered by insulin in vitro. |
| 720 | 8374794 | The antinociceptive effects of beta-endorphin administered i.c.v. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of naltrindole, a selective delta-opioid receptor antagonist. beta-Endorphin administered i.t. also produced a dose-dependent antinociception in both diabetic and non-diabetic mice. |
| 721 | 8382698 | Processing of proopiomelanocortin by insulin secretory granule proinsulin processing endopeptidases. |
| 722 | 8382698 | A lysed preparation of isolated insulin secretory granules efficiently cleaved murine proopiomelanocortin (mPOMC) at physiologically important Lys-Arg processing sites. |
| 723 | 8382698 | The principal peptide hormone products generated by the insulin secretory granule lysate were identified by specific radioimmunoassay and NH2-terminal microsequencing analysis of high performance liquid chromatography-separated products as alpha-melanocyte-stimulating hormone, corticotropin-like intermediate, gamma-lipotropin, beta-endorphin-(1-31), 18-kDa NH2-terminal fragment and, to a lesser extent, adrenocorticotrophin and beta-lipotropin. |
| 724 | 8382698 | The in vitro processing of mPOMC by the insulin secretory granule endopeptidase activity reported here is in excellent agreement with the in vivo processing of this prohormone by a combination of PC2 and PC3, candidates of prohormone endpeptidase, in gene transfer studies with cells that express the regulated secretory pathway (Thomas, L., Leduc, R., Thorne, B. |
| 725 | 8382698 | Processing of proopiomelanocortin by insulin secretory granule proinsulin processing endopeptidases. |
| 726 | 8382698 | A lysed preparation of isolated insulin secretory granules efficiently cleaved murine proopiomelanocortin (mPOMC) at physiologically important Lys-Arg processing sites. |
| 727 | 8382698 | The principal peptide hormone products generated by the insulin secretory granule lysate were identified by specific radioimmunoassay and NH2-terminal microsequencing analysis of high performance liquid chromatography-separated products as alpha-melanocyte-stimulating hormone, corticotropin-like intermediate, gamma-lipotropin, beta-endorphin-(1-31), 18-kDa NH2-terminal fragment and, to a lesser extent, adrenocorticotrophin and beta-lipotropin. |
| 728 | 8382698 | The in vitro processing of mPOMC by the insulin secretory granule endopeptidase activity reported here is in excellent agreement with the in vivo processing of this prohormone by a combination of PC2 and PC3, candidates of prohormone endpeptidase, in gene transfer studies with cells that express the regulated secretory pathway (Thomas, L., Leduc, R., Thorne, B. |
| 729 | 8382698 | Processing of proopiomelanocortin by insulin secretory granule proinsulin processing endopeptidases. |
| 730 | 8382698 | A lysed preparation of isolated insulin secretory granules efficiently cleaved murine proopiomelanocortin (mPOMC) at physiologically important Lys-Arg processing sites. |
| 731 | 8382698 | The principal peptide hormone products generated by the insulin secretory granule lysate were identified by specific radioimmunoassay and NH2-terminal microsequencing analysis of high performance liquid chromatography-separated products as alpha-melanocyte-stimulating hormone, corticotropin-like intermediate, gamma-lipotropin, beta-endorphin-(1-31), 18-kDa NH2-terminal fragment and, to a lesser extent, adrenocorticotrophin and beta-lipotropin. |
| 732 | 8382698 | The in vitro processing of mPOMC by the insulin secretory granule endopeptidase activity reported here is in excellent agreement with the in vivo processing of this prohormone by a combination of PC2 and PC3, candidates of prohormone endpeptidase, in gene transfer studies with cells that express the regulated secretory pathway (Thomas, L., Leduc, R., Thorne, B. |
| 733 | 8382698 | Processing of proopiomelanocortin by insulin secretory granule proinsulin processing endopeptidases. |
| 734 | 8382698 | A lysed preparation of isolated insulin secretory granules efficiently cleaved murine proopiomelanocortin (mPOMC) at physiologically important Lys-Arg processing sites. |
| 735 | 8382698 | The principal peptide hormone products generated by the insulin secretory granule lysate were identified by specific radioimmunoassay and NH2-terminal microsequencing analysis of high performance liquid chromatography-separated products as alpha-melanocyte-stimulating hormone, corticotropin-like intermediate, gamma-lipotropin, beta-endorphin-(1-31), 18-kDa NH2-terminal fragment and, to a lesser extent, adrenocorticotrophin and beta-lipotropin. |
| 736 | 8382698 | The in vitro processing of mPOMC by the insulin secretory granule endopeptidase activity reported here is in excellent agreement with the in vivo processing of this prohormone by a combination of PC2 and PC3, candidates of prohormone endpeptidase, in gene transfer studies with cells that express the regulated secretory pathway (Thomas, L., Leduc, R., Thorne, B. |
| 737 | 8387536 | To understand the mechanism(s) of decreased HPA axis responsiveness to ether stress in cholestasis, we administered corticotropin-releasing factor (CRF) and measured hypothalamic content, mRNA levels and in vitro secretion of CRF and arginine vasopressin (AVP), the two principal secretagogues of ACTH. |
| 738 | 8387536 | In BDR animals, ACTH responses to CRF were decreased and hypothalamic content of CRF and CRF mRNA expression in the paraventricular nucleus were decreased by 25 and 37%, respectively. |
| 739 | 8387536 | These findings demonstrate that acute cholestasis in the rat is associated with suppression of hypothalamic-pituitary-adrenal axis responsiveness to stress and demonstrate a dissociation between mechanisms of ACTH regulation mediated by CRF and AVP. |
| 740 | 8387536 | To understand the mechanism(s) of decreased HPA axis responsiveness to ether stress in cholestasis, we administered corticotropin-releasing factor (CRF) and measured hypothalamic content, mRNA levels and in vitro secretion of CRF and arginine vasopressin (AVP), the two principal secretagogues of ACTH. |
| 741 | 8387536 | In BDR animals, ACTH responses to CRF were decreased and hypothalamic content of CRF and CRF mRNA expression in the paraventricular nucleus were decreased by 25 and 37%, respectively. |
| 742 | 8387536 | These findings demonstrate that acute cholestasis in the rat is associated with suppression of hypothalamic-pituitary-adrenal axis responsiveness to stress and demonstrate a dissociation between mechanisms of ACTH regulation mediated by CRF and AVP. |
| 743 | 8387536 | To understand the mechanism(s) of decreased HPA axis responsiveness to ether stress in cholestasis, we administered corticotropin-releasing factor (CRF) and measured hypothalamic content, mRNA levels and in vitro secretion of CRF and arginine vasopressin (AVP), the two principal secretagogues of ACTH. |
| 744 | 8387536 | In BDR animals, ACTH responses to CRF were decreased and hypothalamic content of CRF and CRF mRNA expression in the paraventricular nucleus were decreased by 25 and 37%, respectively. |
| 745 | 8387536 | These findings demonstrate that acute cholestasis in the rat is associated with suppression of hypothalamic-pituitary-adrenal axis responsiveness to stress and demonstrate a dissociation between mechanisms of ACTH regulation mediated by CRF and AVP. |
| 746 | 8392197 | Pituitary adenylate cyclase-activating polypeptide (PACAP), a neuropeptide belonging to the vasoactive intestinal peptide (VIP)/secretion/glucagon family of peptides, interacts with a distinct high-affinity receptor (type I receptor) on a number of tissues. |
| 747 | 8392197 | These PACAP type I receptors have a high affinity for PACAP and a low affinity for VIP and are present in the hypothalamus and anterior pituitary, where they regulate the release of adrenocorticotropin, luteinizing hormone, growth hormone, and prolactin, and in the adrenal medulla, where they regulate the release of epinephrine. |
| 748 | 8392197 | Here we report the molecular cloning and functional expression of the PACAP type I receptor isolated from an AR4-2J cell cDNA library by cross-hybridization screening with a rat VIP receptor cDNA. |
| 749 | 8397127 | Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. |
| 750 | 8397127 | When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. |
| 751 | 8397127 | The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. |
| 752 | 8397127 | Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. |
| 753 | 8401557 | One week after the operation plasma adrenocorticotropin and prolactin levels were in the control range while plasma alpha-melanocyte-stimulating hormone was elevated. |
| 754 | 8406339 | During periods of 1-5 years per child, the following abnormalities developed: diabetes insipidus (n = 5), osmoreceptor dysfunction (hypernatraemia with absent thirst) (n = 3), hyperprolactinaemia (n = 3), growth hormone (GH) deficiency (n = 4, of whom 3 had normal linear growth), ACTH deficiency (n = 2), TSH deficiency (n = 2) and precocious puberty (n = 1, female). |
| 755 | 8412766 | Adrenal steroid and adrenocorticotropin responses to human corticotropin-releasing hormone stimulation test in adolescents with type I diabetes mellitus. |
| 756 | 8412766 | To determine whether abnormalities of hypothalamic-pituitary-adrenal axis function occur in type I diabetes mellitus, corticotropin, cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), and DHEA sulfate (DS) levels were measured after an intravenous (IV) injection of 1 microgram/kg human corticotropin-releasing hormone (CRH) in diabetic adolescents and normal age-matched subjects. |
| 757 | 8412766 | CRH produced a consistent increase in corticotropin blood levels that was comparable in the two groups. |
| 758 | 8412766 | In conclusion, patients with type I diabetes have a discrete response of adrenal steroids to CRH stimulation that appears to be independent of corticotropin secretion. |
| 759 | 8412766 | This phenomenon might be related to a direct effect of insulin on enzyme systems involved in the biosynthetic pathway of adrenal steroids or, alternatively, to an intra-adrenal CRH/corticotropin mechanism acting on the adrenal cortex in a paracrine manner. |
| 760 | 8412766 | Adrenal steroid and adrenocorticotropin responses to human corticotropin-releasing hormone stimulation test in adolescents with type I diabetes mellitus. |
| 761 | 8412766 | To determine whether abnormalities of hypothalamic-pituitary-adrenal axis function occur in type I diabetes mellitus, corticotropin, cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), and DHEA sulfate (DS) levels were measured after an intravenous (IV) injection of 1 microgram/kg human corticotropin-releasing hormone (CRH) in diabetic adolescents and normal age-matched subjects. |
| 762 | 8412766 | CRH produced a consistent increase in corticotropin blood levels that was comparable in the two groups. |
| 763 | 8412766 | In conclusion, patients with type I diabetes have a discrete response of adrenal steroids to CRH stimulation that appears to be independent of corticotropin secretion. |
| 764 | 8412766 | This phenomenon might be related to a direct effect of insulin on enzyme systems involved in the biosynthetic pathway of adrenal steroids or, alternatively, to an intra-adrenal CRH/corticotropin mechanism acting on the adrenal cortex in a paracrine manner. |
| 765 | 8412766 | Adrenal steroid and adrenocorticotropin responses to human corticotropin-releasing hormone stimulation test in adolescents with type I diabetes mellitus. |
| 766 | 8412766 | To determine whether abnormalities of hypothalamic-pituitary-adrenal axis function occur in type I diabetes mellitus, corticotropin, cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), and DHEA sulfate (DS) levels were measured after an intravenous (IV) injection of 1 microgram/kg human corticotropin-releasing hormone (CRH) in diabetic adolescents and normal age-matched subjects. |
| 767 | 8412766 | CRH produced a consistent increase in corticotropin blood levels that was comparable in the two groups. |
| 768 | 8412766 | In conclusion, patients with type I diabetes have a discrete response of adrenal steroids to CRH stimulation that appears to be independent of corticotropin secretion. |
| 769 | 8412766 | This phenomenon might be related to a direct effect of insulin on enzyme systems involved in the biosynthetic pathway of adrenal steroids or, alternatively, to an intra-adrenal CRH/corticotropin mechanism acting on the adrenal cortex in a paracrine manner. |
| 770 | 8412766 | Adrenal steroid and adrenocorticotropin responses to human corticotropin-releasing hormone stimulation test in adolescents with type I diabetes mellitus. |
| 771 | 8412766 | To determine whether abnormalities of hypothalamic-pituitary-adrenal axis function occur in type I diabetes mellitus, corticotropin, cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), and DHEA sulfate (DS) levels were measured after an intravenous (IV) injection of 1 microgram/kg human corticotropin-releasing hormone (CRH) in diabetic adolescents and normal age-matched subjects. |
| 772 | 8412766 | CRH produced a consistent increase in corticotropin blood levels that was comparable in the two groups. |
| 773 | 8412766 | In conclusion, patients with type I diabetes have a discrete response of adrenal steroids to CRH stimulation that appears to be independent of corticotropin secretion. |
| 774 | 8412766 | This phenomenon might be related to a direct effect of insulin on enzyme systems involved in the biosynthetic pathway of adrenal steroids or, alternatively, to an intra-adrenal CRH/corticotropin mechanism acting on the adrenal cortex in a paracrine manner. |
| 775 | 8412766 | Adrenal steroid and adrenocorticotropin responses to human corticotropin-releasing hormone stimulation test in adolescents with type I diabetes mellitus. |
| 776 | 8412766 | To determine whether abnormalities of hypothalamic-pituitary-adrenal axis function occur in type I diabetes mellitus, corticotropin, cortisol, 17-hydroxyprogesterone (17-OHP), androstenedione (D4-A), dehydroepiandrosterone (DHEA), and DHEA sulfate (DS) levels were measured after an intravenous (IV) injection of 1 microgram/kg human corticotropin-releasing hormone (CRH) in diabetic adolescents and normal age-matched subjects. |
| 777 | 8412766 | CRH produced a consistent increase in corticotropin blood levels that was comparable in the two groups. |
| 778 | 8412766 | In conclusion, patients with type I diabetes have a discrete response of adrenal steroids to CRH stimulation that appears to be independent of corticotropin secretion. |
| 779 | 8412766 | This phenomenon might be related to a direct effect of insulin on enzyme systems involved in the biosynthetic pathway of adrenal steroids or, alternatively, to an intra-adrenal CRH/corticotropin mechanism acting on the adrenal cortex in a paracrine manner. |
| 780 | 8485640 | A variety of endocrinological abnormalities, relevant to both pathogenesis and diagnosis, may be demonstrated in equine Cushing's disease, including hyperadrenocorticism, peripheral insulin resistance and excessive POMC-peptide secretion from the pituitary gland. |
| 781 | 8531185 | Central diabetes insipidus in a dog with a pro-opiomelanocortin-producing pituitary tumor not causing hyperadrenocorticism. |
| 782 | 8539261 | Regulation of insulin-like growth factor-binding proteins in rats with insulin-dependent diabetes mellitus. |
| 783 | 8539261 | As previously reported, activation of the adrenocorticotropic hormone (ACTH)-adrenal cortical axis in rats with insulin-dependent diabetes mellitus (IDDM) reduces their growth and circulating insulin-like growth factor-I (IGF-I) levels and induces a resistance to growth hormone (GH) and IGF-I. |
| 784 | 8539261 | Induction of IDDM increased serum concentrations of IGFBP-1 and -2 and reduced those of IGFBP-3 and -4. |
| 785 | 8539261 | Although serum IGFBP-1 and -2 concentrations remained elevated in the HxDb rats compared with the NonDb controls, IGFBP-1 levels were reduced compared with those in the Db controls. |
| 786 | 8539261 | Serum IGFBP-3 and -4 were reduced to levels below those in Db controls. |
| 787 | 8539261 | Although IGFBP-3 and -4 concentrations were elevated to normal in AxDb rats, the IGFBP-2 concentration was increased above those in both NonDb and Db rats and the IGFBP-1 concentration was reduced. |
| 788 | 8539261 | Administration of pGH increased serum IGFBP-4 concentrations in all groups and IGFBP-3 concentrations in all groups except the Db. |
| 789 | 8539261 | The refractoriness of Db rats to pGH is associated with a failure of the hormone to elevate IGFBP-2 and -3 titers and to reduce those of IGFBP-1. |
| 790 | 8539261 | Impaired growth was associated with substantially reduced IGFBP-3 concentrations and elevated IGFBP-1, whereas growth restoration was associated with the opposite changes. |
| 791 | 8593805 | To determine the effects of PSC on hypothalamic and pituitary function, VP and CRH receptors and POMC messenger RNA (mRNA) in the pituitary, and CRH, VP, and OT mRNA levels in the PVN were examined in 7-day PSC and sham-operated rats. |
| 792 | 8593805 | Plasma ACTH and corticosterone levels were significantly increased by PSC, an effect that was attenuated by minipump infusion of desamino-[D-Arg8]-vasopressin (DDAVP) given to correct the diabetes insipidus. [3H]VP binding to anterior pituitary membranes from PSC rats was reduced by 50% compared to that in sham-operated controls, but VP V1b receptor mRNA levels measured by in situ hybridization were unchanged. |
| 793 | 8593805 | Correction of the diabetes insipidus by DDAVP treatment further decreased hypothalamic VP mRNA levels, but restored CRH mRNA to control levels. |
| 794 | 8593805 | To determine the effects of PSC on hypothalamic and pituitary function, VP and CRH receptors and POMC messenger RNA (mRNA) in the pituitary, and CRH, VP, and OT mRNA levels in the PVN were examined in 7-day PSC and sham-operated rats. |
| 795 | 8593805 | Plasma ACTH and corticosterone levels were significantly increased by PSC, an effect that was attenuated by minipump infusion of desamino-[D-Arg8]-vasopressin (DDAVP) given to correct the diabetes insipidus. [3H]VP binding to anterior pituitary membranes from PSC rats was reduced by 50% compared to that in sham-operated controls, but VP V1b receptor mRNA levels measured by in situ hybridization were unchanged. |
| 796 | 8593805 | Correction of the diabetes insipidus by DDAVP treatment further decreased hypothalamic VP mRNA levels, but restored CRH mRNA to control levels. |
| 797 | 8597446 | At the level of the CNS, insulin inhibits and corticosteroids stimulate expression of NPY mRNA in the arcuate nuclei, and these actions may explain, in part, the reciprocal actions of the hormones on energy acquisition. |
| 798 | 8597446 | By contrast, NPY injected ivt stimulates identical ACTH responses in the AM in fed rats and in rats fasted overnight, suggesting that NPY acts to stimulate CRF secretion at a site closer to the PVN than the stress of restraint, which is filtered through the neural energy balance system. |
| 799 | 8606627 | Increased levels of secondary hormones, such as gastrin (4 patients), vasoactive intestinal peptide (1 patient), serotonin (5 patients), insulin (6 patients, clinically significant in 1 only), human pancreatic polypeptide (2 patients), calcitonin (2 patients) and adrenocorticotropic hormone (2 patients), contributed to clinical symptoms leading to the diagnosis of an islet cell tumor before the onset of the full glucagonoma syndrome in 2 patients. |
| 800 | 8636289 | The epinephrine and cortisol responses to hypoglycemia are reduced in insulin-dependent diabetes mellitus (IDDM) patients in strict glycemic control. |
| 801 | 8636289 | To examine this question, we measured counterregulatory hormone secretion during a 3-h hypoglycemic hyperinsulinemic clamp (12 pmol/kg.min) that lowered glucose from 5.0 to 2.2 mmol/L in steps of 0.55 mmol/L every 30 min in 13 well controlled IDDM subjects (hemoglobin A1, 7.8 +/- 0.2%), 14 poorly controlled IDDM subjects (hemoglobin A1, 12.3 +/- 1.5%), and 20 healthy volunteers. |
| 802 | 8636289 | At the nadir glucose level (2.2 mmol/L), ACTH, cortisol, and epinephrine levels were significantly lower in well controlled IDDM compared to healthy controls, and the glucose levels required for significant secretion of ACTH, cortisol, and epinephrine also were lower in well controlled IDDM compared to those in both poorly controlled IDDM and healthy volunteers (P < 0.05). |
| 803 | 8636289 | We conclude that 1) ACTH, cortisol, and epinephrine responses during hypoglycemia are reduced in IDDM patients in strict glycemic control; 2) the lower cortisol response is correlated with reduced ACTH levels; and 3) in healthy subjects, the cortisol response to hypoglycemia is abolished by adrenocortical blockade with metyrapone, whereas the epinephrine response to hypoglycemia remains intact. |
| 804 | 8636289 | The epinephrine and cortisol responses to hypoglycemia are reduced in insulin-dependent diabetes mellitus (IDDM) patients in strict glycemic control. |
| 805 | 8636289 | To examine this question, we measured counterregulatory hormone secretion during a 3-h hypoglycemic hyperinsulinemic clamp (12 pmol/kg.min) that lowered glucose from 5.0 to 2.2 mmol/L in steps of 0.55 mmol/L every 30 min in 13 well controlled IDDM subjects (hemoglobin A1, 7.8 +/- 0.2%), 14 poorly controlled IDDM subjects (hemoglobin A1, 12.3 +/- 1.5%), and 20 healthy volunteers. |
| 806 | 8636289 | At the nadir glucose level (2.2 mmol/L), ACTH, cortisol, and epinephrine levels were significantly lower in well controlled IDDM compared to healthy controls, and the glucose levels required for significant secretion of ACTH, cortisol, and epinephrine also were lower in well controlled IDDM compared to those in both poorly controlled IDDM and healthy volunteers (P < 0.05). |
| 807 | 8636289 | We conclude that 1) ACTH, cortisol, and epinephrine responses during hypoglycemia are reduced in IDDM patients in strict glycemic control; 2) the lower cortisol response is correlated with reduced ACTH levels; and 3) in healthy subjects, the cortisol response to hypoglycemia is abolished by adrenocortical blockade with metyrapone, whereas the epinephrine response to hypoglycemia remains intact. |
| 808 | 8641721 | Moreover, AII acts on the central receptors to stimulate AVP and ACTH secretion, drinking and peripherally increase synthesis and secretion of aldosterone. |
| 809 | 8710916 | Transgenic nonobese diabetic mice were created in which insulin expression was targeted to proopiomelanocortin-expressing pituitary cells. |
| 810 | 8710916 | Proopiomelanocortin-expressing intermediate lobe pituitary cells efficiently secrete fully processed, mature insulin via a regulated secretory pathway, similar to islet beta cells. |
| 811 | 8710916 | Transgenic nonobese diabetic mice were created in which insulin expression was targeted to proopiomelanocortin-expressing pituitary cells. |
| 812 | 8710916 | Proopiomelanocortin-expressing intermediate lobe pituitary cells efficiently secrete fully processed, mature insulin via a regulated secretory pathway, similar to islet beta cells. |
| 813 | 8738484 | Remission of disease was achieved in 81%, 77%, 91%, and 100% of GH-, PRL-, ACTH-, and TSH-secreting adenomas, respectively. |
| 814 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 815 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 816 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 817 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 818 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 819 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 820 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 821 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 822 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 823 | 8741254 | Immunohistochemical studies showed positive reaction for S-100 protein in the tumor cell nuclei, but no reaction for glial fibrillary acidic protein, neurofilament protein, Leu-7, oxytocin, beta-endorphin, adrenocorticotropic hormone, and vimentin. |
| 824 | 8750568 | We administered a recently developed neuroendocrine function test that combines dexamethasone suppression (1.5 mg orally at 2300 h) and corticotropin-releasing hormone (CRH) stimulation (100 micrograms i.v. at 1500 h the following day) and measured the response of plasma cortisol and corticotrophin (ACTH) secretion in 19 patients with an acute exacerbation of MS. |
| 825 | 8777245 | Umbilical cord dopamine beta-hydroxylase, chromogranin A and met-enkephalin after conditions associated with chronic intrauterine stress. |
| 826 | 8781292 | We measured plasma met-enkephalin (met-Enk) levels in eight neuropathic (four with insulin-dependent diabetes mellitus [IDDM] and four with non-insulin-dependent diabetes mellitus [NIDDM]) and eight nonneuropathic (four IDDM and four NIDDM) diabetic patients to study met-Enk secretion in diabetic patients with asymptomatic autonomic neuropathy. |
| 827 | 8815789 | Germline loss of function mutations in rhodopsin, cone opsins, the V2 vasopressin receptor, ACTH receptor, and calcium-sensing receptor are responsible for retinitis pigmentosa, color blindness, nephrogenic diabetes insipidus, familial ACTH resistance, and familial hypocalciuric hypercalcemia, respectively. |
| 828 | 8817849 | Immunohistochemical staining for growth hormone, adrenocorticotropic hormone, and prolactin showed a strong immunolabeling for growth hormone within the cytoplasm of the tumor cells. |
| 829 | 8888355 | Effects of corticotropin-releasing hormone on ACTH, cortisol and 13, 14-dihydro-15-keto prostaglandin E2 in patients with diabetes insipidus before and after captopril treatment. |
| 830 | 8888355 | A corticotropin-releasing hormone (CRH) test was performed on 7 patients with central diabetes insipidus (DI) and on 7 healthy subjects. |
| 831 | 8888355 | The short-term captopril treatment resulted in a significant decrease of both basal and CRH-stimulated ACTH and cortisol levels in the patients with DI. |
| 832 | 8888355 | Angiotensin II (A II) is involved in the regulation of ACTH. |
| 833 | 8888355 | Effects of corticotropin-releasing hormone on ACTH, cortisol and 13, 14-dihydro-15-keto prostaglandin E2 in patients with diabetes insipidus before and after captopril treatment. |
| 834 | 8888355 | A corticotropin-releasing hormone (CRH) test was performed on 7 patients with central diabetes insipidus (DI) and on 7 healthy subjects. |
| 835 | 8888355 | The short-term captopril treatment resulted in a significant decrease of both basal and CRH-stimulated ACTH and cortisol levels in the patients with DI. |
| 836 | 8888355 | Angiotensin II (A II) is involved in the regulation of ACTH. |
| 837 | 8888355 | Effects of corticotropin-releasing hormone on ACTH, cortisol and 13, 14-dihydro-15-keto prostaglandin E2 in patients with diabetes insipidus before and after captopril treatment. |
| 838 | 8888355 | A corticotropin-releasing hormone (CRH) test was performed on 7 patients with central diabetes insipidus (DI) and on 7 healthy subjects. |
| 839 | 8888355 | The short-term captopril treatment resulted in a significant decrease of both basal and CRH-stimulated ACTH and cortisol levels in the patients with DI. |
| 840 | 8888355 | Angiotensin II (A II) is involved in the regulation of ACTH. |
| 841 | 8915692 | We extracted gammaglobulins from the serum of 10 patients with insulin-dependent diabetes mellitus (IDDM) to investigate their effect on anterior pituitary hormone secretion using cultures of rat anterior pituitary cells. |
| 842 | 8915692 | The gammaglobulin from each of the 3 patients with PGA and an isolated failure of secretion of adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH) or gonadotropin inhibited the secretion of ACTH, TSH or gonadotropin in cultures of rat anterior pituitary cells. |
| 843 | 8928409 | The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. |
| 844 | 8930533 | After delivery, plasma levels of PRL, ACTH and cortisol decreased markedly. |
| 845 | 8930533 | Because pituitary function tests indicated that ACTH, PRL, GH and TSH were of low levels, hydrocortisone and L-thyroxine were orally administered. |
| 846 | 8930533 | After delivery, plasma levels of PRL, ACTH and cortisol decreased markedly. |
| 847 | 8930533 | Because pituitary function tests indicated that ACTH, PRL, GH and TSH were of low levels, hydrocortisone and L-thyroxine were orally administered. |
| 848 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 849 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 850 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 851 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 852 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 853 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 854 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 855 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 856 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 857 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 858 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 859 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 860 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 861 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 862 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 863 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 864 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 865 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 866 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 867 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 868 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 869 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 870 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 871 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 872 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 873 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 874 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 875 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 876 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 877 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 878 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 879 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 880 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 881 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 882 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 883 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 884 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 885 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 886 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 887 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 888 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 889 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 890 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 891 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 892 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 893 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 894 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 895 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 896 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 897 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 898 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 899 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 900 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 901 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 902 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 903 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 904 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 905 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 906 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 907 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 908 | 8931651 | Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus. |
| 909 | 8931651 | Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. |
| 910 | 8931651 | In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. |
| 911 | 8931651 | The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. |
| 912 | 8931651 | The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). |
| 913 | 8931651 | During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). |
| 914 | 8931651 | The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). |
| 915 | 8931651 | The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). |
| 916 | 8931651 | The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). |
| 917 | 8931651 | In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. |
| 918 | 8939064 | The genes at these loci include agouti, which encodes a molecule that antagonizes the binding of alpha melanocyte-stimulating hormone to its receptor; fat, which encodes carboxypeptidase E; tubby, which encodes a putative phosphodiesterase; obese, which encodes a circulating satiety protein; and diabetes, which encodes the receptor for the obese gene product. |
| 919 | 8961238 | These shared symptoms include elevated tumour necrosis factor-alpha, down-regulated interleukin-2 and interleukin-4 and depletion of lean body mass. |
| 920 | 8961238 | Furthermore, the following neuropeptides are dysregulated in both anorexia nervosa and cancer cachexia: vasoactive intestinal peptide, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, peptide YY and beta-endorphin. |
| 921 | 8983089 | During the test and on a control day, heart rate, blood pressure, plasma ACTH, cortisol, catecholamines and prolactin were measured. |
| 922 | 9019408 | We show that in the Cpe(fat) mutant mouse lacking CPE, the pituitary prohormone, pro-opiomelanocortin, was missorted to the constitutive pathway and secreted in an unregulated manner. |
| 923 | 9026270 | In an attempt to define the hypothalamic-pituitary-adrenal (HPA) axis in non-insulin dependent diabetic rats (WBN/Kob), we measured plasma corticotropin releasing factor (CRF), as well as arginine vasopressin (AVP), ACTH, and corticosterone (B), CRF concentrations in the median eminence (ME), the remainder of the hypothalamus (rHY) and the neurointermediate lobe of the pituitary (NIL). |
| 924 | 9054940 | This region contains several potential candidate genes for obesity, including glucokinase regulatory protein (GCKR) and pro-opiomelanocortin (POMC). |
| 925 | 9063651 | Anterior pituitary function was tested by use of the combined anterior pituitary (CAP) function test, which consisted of sequential 30-sec intravenous injections of four hypothalamic releasing hormones, in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. |
| 926 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 927 | 9063651 | In the CAP test and the haloperidol test, the peaks for the plasma concentrations of ACTH, cortisol, GH, LH, PRL, and alpha-MSH occurred within 45 min after injection. |
| 928 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 929 | 9063651 | It is concluded that 1) stimulation of the anterior pituitary with multiple hypophysiotropic hormones, stimulation of the pars intermedia with a dopamine antagonist, and stimulation of the neurohypophysis with hypertonic saline do not cause side effects that would prohibit routine use, 2) in the routine stimulation of the anterior pituitary and the pars intermedia, blood sampling can be confined to the first 45 min, 3) the ACTH and cortisol responses to hypophysiotropic stimulation are the most sensitive indicators for residual pituitary function after hypophysectomy, 4) small islets of pituitary cells in the sella turcica, containing corticotropic cells, are the most likely source of the attenuated corticotropic response that may occur after hypophysectomy, and 5) residual AVP release from the hypothalamus after hypophysectomy is sufficient to prevent diabetes insipidus, despite the fact that the AVP response to hypertonic saline infusion is completely abolished. |
| 930 | 9063651 | Anterior pituitary function was tested by use of the combined anterior pituitary (CAP) function test, which consisted of sequential 30-sec intravenous injections of four hypothalamic releasing hormones, in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. |
| 931 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 932 | 9063651 | In the CAP test and the haloperidol test, the peaks for the plasma concentrations of ACTH, cortisol, GH, LH, PRL, and alpha-MSH occurred within 45 min after injection. |
| 933 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 934 | 9063651 | It is concluded that 1) stimulation of the anterior pituitary with multiple hypophysiotropic hormones, stimulation of the pars intermedia with a dopamine antagonist, and stimulation of the neurohypophysis with hypertonic saline do not cause side effects that would prohibit routine use, 2) in the routine stimulation of the anterior pituitary and the pars intermedia, blood sampling can be confined to the first 45 min, 3) the ACTH and cortisol responses to hypophysiotropic stimulation are the most sensitive indicators for residual pituitary function after hypophysectomy, 4) small islets of pituitary cells in the sella turcica, containing corticotropic cells, are the most likely source of the attenuated corticotropic response that may occur after hypophysectomy, and 5) residual AVP release from the hypothalamus after hypophysectomy is sufficient to prevent diabetes insipidus, despite the fact that the AVP response to hypertonic saline infusion is completely abolished. |
| 935 | 9063651 | Anterior pituitary function was tested by use of the combined anterior pituitary (CAP) function test, which consisted of sequential 30-sec intravenous injections of four hypothalamic releasing hormones, in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. |
| 936 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 937 | 9063651 | In the CAP test and the haloperidol test, the peaks for the plasma concentrations of ACTH, cortisol, GH, LH, PRL, and alpha-MSH occurred within 45 min after injection. |
| 938 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 939 | 9063651 | It is concluded that 1) stimulation of the anterior pituitary with multiple hypophysiotropic hormones, stimulation of the pars intermedia with a dopamine antagonist, and stimulation of the neurohypophysis with hypertonic saline do not cause side effects that would prohibit routine use, 2) in the routine stimulation of the anterior pituitary and the pars intermedia, blood sampling can be confined to the first 45 min, 3) the ACTH and cortisol responses to hypophysiotropic stimulation are the most sensitive indicators for residual pituitary function after hypophysectomy, 4) small islets of pituitary cells in the sella turcica, containing corticotropic cells, are the most likely source of the attenuated corticotropic response that may occur after hypophysectomy, and 5) residual AVP release from the hypothalamus after hypophysectomy is sufficient to prevent diabetes insipidus, despite the fact that the AVP response to hypertonic saline infusion is completely abolished. |
| 940 | 9063651 | Anterior pituitary function was tested by use of the combined anterior pituitary (CAP) function test, which consisted of sequential 30-sec intravenous injections of four hypothalamic releasing hormones, in the following order and doses: 1 microgram of corticotropin-releasing hormone (CRH)/kg, 1 microgram of growth hormone-releasing hormone (GHRH)/kg, 10 micrograms of gonadotropin-releasing hormone (GnRH)/kg, and 10 micrograms of thyrotropin-releasing hormone (TRH)/kg. |
| 941 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 942 | 9063651 | In the CAP test and the haloperidol test, the peaks for the plasma concentrations of ACTH, cortisol, GH, LH, PRL, and alpha-MSH occurred within 45 min after injection. |
| 943 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 944 | 9063651 | It is concluded that 1) stimulation of the anterior pituitary with multiple hypophysiotropic hormones, stimulation of the pars intermedia with a dopamine antagonist, and stimulation of the neurohypophysis with hypertonic saline do not cause side effects that would prohibit routine use, 2) in the routine stimulation of the anterior pituitary and the pars intermedia, blood sampling can be confined to the first 45 min, 3) the ACTH and cortisol responses to hypophysiotropic stimulation are the most sensitive indicators for residual pituitary function after hypophysectomy, 4) small islets of pituitary cells in the sella turcica, containing corticotropic cells, are the most likely source of the attenuated corticotropic response that may occur after hypophysectomy, and 5) residual AVP release from the hypothalamus after hypophysectomy is sufficient to prevent diabetes insipidus, despite the fact that the AVP response to hypertonic saline infusion is completely abolished. |
| 945 | 9088893 | In view of recent findings of an attenuated response of the hypothalamic-pituitary-adrenal (HPA) system in patients with atopic eczema during a human corticotropin-releasing hormone (hCRH) challenge paradigm fourteen consecutive non-specifically trained in-patients with atopic eczema (8 men, 6 women) and an age-matched control group (8 men, 6 women) performed exhausting incremental graded bicycle exercise to evaluate cortisol, adrenocorticotropin (ACTH), beta-endorphin, epinephrine and norepinephrine releases induced by physical stress. |
| 946 | 9088893 | In contrast to the challenge with exogenous hCRH no substantial difference in the net responses of ACTH and cortisol could be detected between patients with atopic eczema and controls using the physical stress paradigm. |
| 947 | 9088893 | In view of recent findings of an attenuated response of the hypothalamic-pituitary-adrenal (HPA) system in patients with atopic eczema during a human corticotropin-releasing hormone (hCRH) challenge paradigm fourteen consecutive non-specifically trained in-patients with atopic eczema (8 men, 6 women) and an age-matched control group (8 men, 6 women) performed exhausting incremental graded bicycle exercise to evaluate cortisol, adrenocorticotropin (ACTH), beta-endorphin, epinephrine and norepinephrine releases induced by physical stress. |
| 948 | 9088893 | In contrast to the challenge with exogenous hCRH no substantial difference in the net responses of ACTH and cortisol could be detected between patients with atopic eczema and controls using the physical stress paradigm. |
| 949 | 9096167 | In vitro, in heterologous cells expressing either rat MC3-R or MC4-R, the major MCR subtypes expressed in brain, SHU-9119 showed no intrinsic agonism, but it inhibited alpha-MSH-induced cAMP accumulation (IC50 = 0.48 +/- 0.19 and 0.41 +/- 0.28 nM, respectively) and [125I]-[Nle4,DPhe7]-alpha-MSH binding (IC50 = 1.0 +/- 0.1 and 0.9 +/- 0.3 nM, respectively). |
| 950 | 9100602 | Effect of plasma osmolality on pituitary-adrenal responses to corticotropin-releasing hormone and atrial natriuretic peptide changes in central diabetes insipidus. |
| 951 | 9100602 | The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). |
| 952 | 9100602 | The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. |
| 953 | 9100602 | The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 +/- 99 vs. 709 +/- 62 pmol.L/min] and hCRH/5% NaCl (AUC 1602 +/- 209 vs. 1158 +/- 187 pmol.L.min). |
| 954 | 9100602 | The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. |
| 955 | 9100602 | There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). |
| 956 | 9100602 | These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP. |
| 957 | 9100602 | Effect of plasma osmolality on pituitary-adrenal responses to corticotropin-releasing hormone and atrial natriuretic peptide changes in central diabetes insipidus. |
| 958 | 9100602 | The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). |
| 959 | 9100602 | The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. |
| 960 | 9100602 | The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 +/- 99 vs. 709 +/- 62 pmol.L/min] and hCRH/5% NaCl (AUC 1602 +/- 209 vs. 1158 +/- 187 pmol.L.min). |
| 961 | 9100602 | The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. |
| 962 | 9100602 | There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). |
| 963 | 9100602 | These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP. |
| 964 | 9100602 | Effect of plasma osmolality on pituitary-adrenal responses to corticotropin-releasing hormone and atrial natriuretic peptide changes in central diabetes insipidus. |
| 965 | 9100602 | The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). |
| 966 | 9100602 | The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. |
| 967 | 9100602 | The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 +/- 99 vs. 709 +/- 62 pmol.L/min] and hCRH/5% NaCl (AUC 1602 +/- 209 vs. 1158 +/- 187 pmol.L.min). |
| 968 | 9100602 | The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. |
| 969 | 9100602 | There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). |
| 970 | 9100602 | These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP. |
| 971 | 9100602 | Effect of plasma osmolality on pituitary-adrenal responses to corticotropin-releasing hormone and atrial natriuretic peptide changes in central diabetes insipidus. |
| 972 | 9100602 | The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). |
| 973 | 9100602 | The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. |
| 974 | 9100602 | The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 +/- 99 vs. 709 +/- 62 pmol.L/min] and hCRH/5% NaCl (AUC 1602 +/- 209 vs. 1158 +/- 187 pmol.L.min). |
| 975 | 9100602 | The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. |
| 976 | 9100602 | There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). |
| 977 | 9100602 | These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP. |
| 978 | 9134049 | Insulin-dependent diabetes mellitus (IDDM) occurs as a consequence of autoimmune destruction of the insulin-producing pancreatic beta-cells. |
| 979 | 9134049 | Although progress has been made in the field of islet transplantation, an appealing alternative strategy for beta-cell replacement therapy for IDDM is to target insulin expression to non-islet cells. |
| 980 | 9134049 | We have recently generated transgenic nonobese diabetic (NOD) mice in which insulin gene expression was targeted to proopiomelanocortin (POMC)-expressing cells of the intermediate lobe (IL) of the pituitary. |
| 981 | 9134049 | We have shown that POMC-expressing IL pituitary cells secreted large amounts of mature insulin, similar to islet beta-cells. |
| 982 | 9134049 | These features are highly advantageous in the transplantation setting and demonstrate the considerable potential of these non-islet cell types for insulin-gene delivery in IDDM. |
| 983 | 9134049 | Insulin-dependent diabetes mellitus (IDDM) occurs as a consequence of autoimmune destruction of the insulin-producing pancreatic beta-cells. |
| 984 | 9134049 | Although progress has been made in the field of islet transplantation, an appealing alternative strategy for beta-cell replacement therapy for IDDM is to target insulin expression to non-islet cells. |
| 985 | 9134049 | We have recently generated transgenic nonobese diabetic (NOD) mice in which insulin gene expression was targeted to proopiomelanocortin (POMC)-expressing cells of the intermediate lobe (IL) of the pituitary. |
| 986 | 9134049 | We have shown that POMC-expressing IL pituitary cells secreted large amounts of mature insulin, similar to islet beta-cells. |
| 987 | 9134049 | These features are highly advantageous in the transplantation setting and demonstrate the considerable potential of these non-islet cell types for insulin-gene delivery in IDDM. |
| 988 | 9137936 | Corticotropin-releasing factor (CRF) is the primary physiological regulator of basal and stress-induced release of ACTH, beta-endorphin and other POMC-derived peptides from the pituitary and plays a major role in the brain and periphery in coordinating endocrine, electrophysiological, autonomic, behavioral and immune responses to stress. |
| 989 | 9137936 | This review summarizes four decades of research beginning with the search for the factor that governs the release of ACTH and getting to the recent findings including the successful cloning of different receptor subtypes and the discovery of a new endogenous CRF-related ligand. |
| 990 | 9137936 | Corticotropin-releasing factor (CRF) is the primary physiological regulator of basal and stress-induced release of ACTH, beta-endorphin and other POMC-derived peptides from the pituitary and plays a major role in the brain and periphery in coordinating endocrine, electrophysiological, autonomic, behavioral and immune responses to stress. |
| 991 | 9137936 | This review summarizes four decades of research beginning with the search for the factor that governs the release of ACTH and getting to the recent findings including the successful cloning of different receptor subtypes and the discovery of a new endogenous CRF-related ligand. |
| 992 | 9144234 | Intracellular misrouting and abnormal secretion of adrenocorticotropin and growth hormone in cpefat mice associated with a carboxypeptidase E mutation. |
| 993 | 9144234 | Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. |
| 994 | 9144234 | Furthermore, pro-opiomelanocortin was secreted constitutively at high levels, showing no response to stimulation by corticotropin-releasing hormone. |
| 995 | 9144234 | These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice. |
| 996 | 9144234 | Intracellular misrouting and abnormal secretion of adrenocorticotropin and growth hormone in cpefat mice associated with a carboxypeptidase E mutation. |
| 997 | 9144234 | Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. |
| 998 | 9144234 | Furthermore, pro-opiomelanocortin was secreted constitutively at high levels, showing no response to stimulation by corticotropin-releasing hormone. |
| 999 | 9144234 | These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice. |
| 1000 | 9144234 | Intracellular misrouting and abnormal secretion of adrenocorticotropin and growth hormone in cpefat mice associated with a carboxypeptidase E mutation. |
| 1001 | 9144234 | Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. |
| 1002 | 9144234 | Furthermore, pro-opiomelanocortin was secreted constitutively at high levels, showing no response to stimulation by corticotropin-releasing hormone. |
| 1003 | 9144234 | These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice. |
| 1004 | 9144234 | Intracellular misrouting and abnormal secretion of adrenocorticotropin and growth hormone in cpefat mice associated with a carboxypeptidase E mutation. |
| 1005 | 9144234 | Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. |
| 1006 | 9144234 | Furthermore, pro-opiomelanocortin was secreted constitutively at high levels, showing no response to stimulation by corticotropin-releasing hormone. |
| 1007 | 9144234 | These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice. |
| 1008 | 9200662 | The crucial role of glucocorticoids in obesity and insulin resistance and the actions of the OB protein leptin on the hypothalamic-pituitary-adrenal (HPA) axis suggest that there is an important interaction of leptin with the glucocorticoid system. |
| 1009 | 9200662 | The accumulation of P450 17alpha mRNA following incubation with ACTH (10 nmol/l) and leptin (10-1,000 ng/ml) was analyzed by Northern blot. |
| 1010 | 9200662 | Addition of OB protein (10-1,000 ng/ml) led to a dose-dependent reduction of ACTH-stimulated cytochrome P450 17alpha mRNA accumulation (from 80 to 45%), suggesting that leptin regulates adrenal steroidogenesis at the transcriptional level. |
| 1011 | 9218248 | MCR are also found in melanocytic cells and adrenal cortical cells, the classical targets for alpha-MSH and ACTH, respectively, in myelogenous and lymphoid tissues, and in various endocrine and exocrine glands, adipocytes, and in autonomic ganglia. |
| 1012 | 9218248 | A group of five G-protein-associated MCR subtypes, each of which is positively coupled to adenylate cyclase, has been identified. |
| 1013 | 9218248 | Among these, the adrenal ACTH receptor (MC2-R) is selectively activated by ACTH. |
| 1014 | 9218248 | In contrast, the other MCR subtypes (MC1-R, MC3-R, MC4-R, MC5-R) recognize a common group of ligands that includes various forms of MSH as well as ACTH; nevertheless they do exhibit important differences in ligand selectivity. |
| 1015 | 9218248 | Moreover, spontaneous dominant mutations of the agouti gene in several strains of mice lead to its ubiquitous overexpression and produces not only yellow coat color, but also obesity and insulin resistance, perhaps as a result of its antagonism of other MCR subtypes. |
| 1016 | 9218248 | MCR are also found in melanocytic cells and adrenal cortical cells, the classical targets for alpha-MSH and ACTH, respectively, in myelogenous and lymphoid tissues, and in various endocrine and exocrine glands, adipocytes, and in autonomic ganglia. |
| 1017 | 9218248 | A group of five G-protein-associated MCR subtypes, each of which is positively coupled to adenylate cyclase, has been identified. |
| 1018 | 9218248 | Among these, the adrenal ACTH receptor (MC2-R) is selectively activated by ACTH. |
| 1019 | 9218248 | In contrast, the other MCR subtypes (MC1-R, MC3-R, MC4-R, MC5-R) recognize a common group of ligands that includes various forms of MSH as well as ACTH; nevertheless they do exhibit important differences in ligand selectivity. |
| 1020 | 9218248 | Moreover, spontaneous dominant mutations of the agouti gene in several strains of mice lead to its ubiquitous overexpression and produces not only yellow coat color, but also obesity and insulin resistance, perhaps as a result of its antagonism of other MCR subtypes. |
| 1021 | 9218248 | MCR are also found in melanocytic cells and adrenal cortical cells, the classical targets for alpha-MSH and ACTH, respectively, in myelogenous and lymphoid tissues, and in various endocrine and exocrine glands, adipocytes, and in autonomic ganglia. |
| 1022 | 9218248 | A group of five G-protein-associated MCR subtypes, each of which is positively coupled to adenylate cyclase, has been identified. |
| 1023 | 9218248 | Among these, the adrenal ACTH receptor (MC2-R) is selectively activated by ACTH. |
| 1024 | 9218248 | In contrast, the other MCR subtypes (MC1-R, MC3-R, MC4-R, MC5-R) recognize a common group of ligands that includes various forms of MSH as well as ACTH; nevertheless they do exhibit important differences in ligand selectivity. |
| 1025 | 9218248 | Moreover, spontaneous dominant mutations of the agouti gene in several strains of mice lead to its ubiquitous overexpression and produces not only yellow coat color, but also obesity and insulin resistance, perhaps as a result of its antagonism of other MCR subtypes. |
| 1026 | 9227842 | Effect of posterior pituitary denervation (PPD) on prolactin (PRL) and alpha-melanocyte-stimulating hormone (alpha-MSH) secretion of lactating rats. |
| 1027 | 9227842 | Denervation of the PP (PPD) is an effective method for having a selective lesion of the innervation of PP, indeed, PPD results in a disappearance of neurosecretory materials from NL and tyrosine hydroxylase (TH) immunoreactivity from IL, leaving blood supply of all three lobes intact. |
| 1028 | 9227842 | PPD blocks separation-induced depletion but only attenuates suckling induced release of PRL. |
| 1029 | 9227842 | Lack of the separation-induced depression in plasma PRL of PPD animals can be partially restored by normalizing the diabetes insipidus with treatment of a vasopressin analogue, 1-desamino-8-D-arginine-vasopressin (dDAVP). |
| 1030 | 9227842 | In contrast, dDAVP, neither alone nor in combination with oxytocin (OXY), can change PPD-induced elevation of plasma alpha-MSH as well as attenuation of PRL response induced by suckling. |
| 1031 | 9227842 | It is concluded that: (1) contribution of the THDA system parallel to the confirmed role in the regulation of alpha-MSH seems to be crucial for the depletion of plasma PRL induced by separation but not for the elevation due to suckling stimulus, (2) intact hypothalamic innervations of both NL and IL, regulating water intake and the secretion of alpha-MSH, respectively, are necessary for normal secretory responses of AL during lactation, (3) as well as for the presence of PRF activity in PP, (4) which does not solely responsible for suckling-induced PRL release. |
| 1032 | 9227842 | Effect of posterior pituitary denervation (PPD) on prolactin (PRL) and alpha-melanocyte-stimulating hormone (alpha-MSH) secretion of lactating rats. |
| 1033 | 9227842 | Denervation of the PP (PPD) is an effective method for having a selective lesion of the innervation of PP, indeed, PPD results in a disappearance of neurosecretory materials from NL and tyrosine hydroxylase (TH) immunoreactivity from IL, leaving blood supply of all three lobes intact. |
| 1034 | 9227842 | PPD blocks separation-induced depletion but only attenuates suckling induced release of PRL. |
| 1035 | 9227842 | Lack of the separation-induced depression in plasma PRL of PPD animals can be partially restored by normalizing the diabetes insipidus with treatment of a vasopressin analogue, 1-desamino-8-D-arginine-vasopressin (dDAVP). |
| 1036 | 9227842 | In contrast, dDAVP, neither alone nor in combination with oxytocin (OXY), can change PPD-induced elevation of plasma alpha-MSH as well as attenuation of PRL response induced by suckling. |
| 1037 | 9227842 | It is concluded that: (1) contribution of the THDA system parallel to the confirmed role in the regulation of alpha-MSH seems to be crucial for the depletion of plasma PRL induced by separation but not for the elevation due to suckling stimulus, (2) intact hypothalamic innervations of both NL and IL, regulating water intake and the secretion of alpha-MSH, respectively, are necessary for normal secretory responses of AL during lactation, (3) as well as for the presence of PRF activity in PP, (4) which does not solely responsible for suckling-induced PRL release. |
| 1038 | 9227842 | Effect of posterior pituitary denervation (PPD) on prolactin (PRL) and alpha-melanocyte-stimulating hormone (alpha-MSH) secretion of lactating rats. |
| 1039 | 9227842 | Denervation of the PP (PPD) is an effective method for having a selective lesion of the innervation of PP, indeed, PPD results in a disappearance of neurosecretory materials from NL and tyrosine hydroxylase (TH) immunoreactivity from IL, leaving blood supply of all three lobes intact. |
| 1040 | 9227842 | PPD blocks separation-induced depletion but only attenuates suckling induced release of PRL. |
| 1041 | 9227842 | Lack of the separation-induced depression in plasma PRL of PPD animals can be partially restored by normalizing the diabetes insipidus with treatment of a vasopressin analogue, 1-desamino-8-D-arginine-vasopressin (dDAVP). |
| 1042 | 9227842 | In contrast, dDAVP, neither alone nor in combination with oxytocin (OXY), can change PPD-induced elevation of plasma alpha-MSH as well as attenuation of PRL response induced by suckling. |
| 1043 | 9227842 | It is concluded that: (1) contribution of the THDA system parallel to the confirmed role in the regulation of alpha-MSH seems to be crucial for the depletion of plasma PRL induced by separation but not for the elevation due to suckling stimulus, (2) intact hypothalamic innervations of both NL and IL, regulating water intake and the secretion of alpha-MSH, respectively, are necessary for normal secretory responses of AL during lactation, (3) as well as for the presence of PRF activity in PP, (4) which does not solely responsible for suckling-induced PRL release. |
| 1044 | 9228515 | In order to clarify the effect of exogenous corticotropin-releasing factor (CRF) on catecholaminergic and serotoninergic system activity in the mediobasal hypothalamus-median eminence (MBH-ME) of ewes the changes in extracellular levels of noradrenaline (NA) and serotonin (5HT), and main metabolites of monoamines, 4-hydroxy-3-methoxyphenylglycol (MHPG), 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanilic acid (HVA), and 5-hydroxy-indolo-3-acetic acid (5-HIAA) were quantified in the perfusates collected from MBH-ME. |
| 1045 | 9228515 | CRF induced a rise in extracellular concentration of NA and 5-HT only in the estrous ewes prior to a preovulatory LH surge. |
| 1046 | 9228515 | CRF treatment caused a heterogenous effect on extra-cellular concentrations of 5-HT in ewes during the preovulatory LH surge. |
| 1047 | 9228515 | It is suggested that: 1) the responses of monoaminergic systems activity in the MBH-ME to CRF in large degree is dependent upon physiological state of ewes and 2) in some endocrinological phases CRF may affect LHRH and other hypothalamic hormone secretion indirectly by altering monoaminergic system activity in the MBH-ME. |
| 1048 | 9278579 | The secreted agouti protein antagonizes the binding of the alpha-melanocyte-stimulating hormone to its receptor (melanocortin 1 receptor) on the surface of hair bulb melanocytes, causing alterations in intracellular cAMP levels. |
| 1049 | 9328209 | In this study, we observed that liberators of NO such as S-nitroso-N-acetyl-penicillamine (SNAP), sodium nitroprusside (Snp) and spermine nonoate (SNO) could significantly inhibit angiotensin II (AII) and ACTH-induced aldosterone synthesis in isolated rat and cultured human adrenal glomerulosa cells. |
| 1050 | 9354856 | Corticosterone response to BrdU was partially reversed by the ACTH-receptor antagonist corticotropin-inhibiting peptide (CIP), and aldosterone response by the arginine vasopressin (AVP) V1-receptor antagonist [amino-Pen1, Val4,D-Arg8]-vasopressin (AVP-A). |
| 1051 | 9354856 | The angiotensin-II (ANG-II)-receptor antagonist [Sar1, Val5, Ala8]-ANG-II (SAR) was ineffective. |
| 1052 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1053 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1054 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1055 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1056 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1057 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1058 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1059 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1060 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1061 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1062 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1063 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1064 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1065 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1066 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1067 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1068 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1069 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1070 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1071 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1072 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1073 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1074 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1075 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1076 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1077 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1078 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1079 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1080 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1081 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1082 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1083 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1084 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1085 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1086 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1087 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1088 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1089 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1090 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1091 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1092 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1093 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1094 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1095 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1096 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1097 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1098 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1099 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1100 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1101 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1102 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1103 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1104 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1105 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1106 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1107 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1108 | 9392508 | Leptin increases hypothalamic pro-opiomelanocortin mRNA expression in the rostral arcuate nucleus. |
| 1109 | 9392508 | Melanocortins are peptides, cleaved from the pro-opiomelanocortin (POMC) precursor, that act in the brain to reduce food intake and are potential mediators of leptin action. |
| 1110 | 9392508 | To test the hypothesis that these POMC neurons are regulated by leptin, we used in situ hybridization to determine whether reduced leptin signaling (as occurs in fasting), genetic leptin deficiency (in obese ob/ob mice), or genetic leptin resistance (in obese db/db mice) lower expression of POMC mRNA. |
| 1111 | 9392508 | We further hypothesized that leptin administration would raise hypothalamic POMC mRNA levels in leptin-deficient animals, but not in mice with defective leptin receptors. |
| 1112 | 9392508 | Five daily intraperitoneal injections of recombinant murine leptin (150 microg) raised levels of POMC mRNA in the rostral arcuate nucleus of ob/ob mice (n = 8) by 73% over saline-treated ob/ob control values (n = 8; P < 0.01), but was without effect in db/db mice (n = 6). |
| 1113 | 9392508 | In normal rats, two injections of a low dose of leptin (3.5 microg) into the third cerebral ventricle (n = 15) during a 40-h period of fasting also increased POMC mRNA levels in the rostral arcuate nucleus to values 39% greater than those in vehicle-treated controls (n = 14; P = 0.02). |
| 1114 | 9392508 | We conclude that reduced central nervous system leptin signaling owing to fasting or to genetic defects in leptin or its receptor lower POMC mRNA levels in the rostral arcuate nucleus. |
| 1115 | 9392508 | The finding that leptin reverses this effect in ob/ob, but not db/db, mice suggests that leptin stimulates arcuate nucleus POMC gene expression via a pathway involving leptin receptors. |
| 1116 | 9404305 | In the group given MPA the increase of ACTH after stimulation with corticotrophin-releasing hormone (CRH) remained normal but it was suppressed in the group treated with PROL. |
| 1117 | 9404305 | The inhibition constants (Ki) of PROL for both the progesterone receptor (PR) and the glucocorticoid receptor (GR) were approximately then times higher than those of MPA. |
| 1118 | 9435421 | Standard and low-dose short adrenocorticotropin test compared with insulin-induced hypoglycemia for assessment of the hypothalamic-pituitary-adrenal axis in children with idiopathic multiple pituitary hormone deficiencies. |
| 1119 | 9439934 | The tumour cells showed immunoreactivity for neuron-specific enolase (NSE), ACTH and beta-endorphin with differing degree of intensity. |
| 1120 | 9519731 | Since alpha-MSH is coded for by the pro-opiomelanocortin (POMC) gene, we examined if POMC gene expression would be inhibited by fasting in normal mice or in models of obesity characterized by leptin insufficiency (ob/ob) or leptin insensitivity (db/db). |
| 1121 | 9519731 | In wild-type mice, hypothalamic POMC mRNA was decreased > 60% after a 2-day fast and was positively correlated with leptin mRNA. |
| 1122 | 9519731 | POMC mRNA was negatively correlated with both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) mRNA. |
| 1123 | 9519731 | Finally, treatment of both male and female ob/ob mice with leptin stimulated hypothalamic POMC mRNA by about threefold. |
| 1124 | 9519731 | These results suggest that impairment in production, processing, or responsiveness to alpha-MSH may be a common feature of obesity and that hypothalamic POMC neurons, stimulated by leptin, may constitute a link between leptin and the melanocortin system. |
| 1125 | 9519731 | Since alpha-MSH is coded for by the pro-opiomelanocortin (POMC) gene, we examined if POMC gene expression would be inhibited by fasting in normal mice or in models of obesity characterized by leptin insufficiency (ob/ob) or leptin insensitivity (db/db). |
| 1126 | 9519731 | In wild-type mice, hypothalamic POMC mRNA was decreased > 60% after a 2-day fast and was positively correlated with leptin mRNA. |
| 1127 | 9519731 | POMC mRNA was negatively correlated with both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) mRNA. |
| 1128 | 9519731 | Finally, treatment of both male and female ob/ob mice with leptin stimulated hypothalamic POMC mRNA by about threefold. |
| 1129 | 9519731 | These results suggest that impairment in production, processing, or responsiveness to alpha-MSH may be a common feature of obesity and that hypothalamic POMC neurons, stimulated by leptin, may constitute a link between leptin and the melanocortin system. |
| 1130 | 9519731 | Since alpha-MSH is coded for by the pro-opiomelanocortin (POMC) gene, we examined if POMC gene expression would be inhibited by fasting in normal mice or in models of obesity characterized by leptin insufficiency (ob/ob) or leptin insensitivity (db/db). |
| 1131 | 9519731 | In wild-type mice, hypothalamic POMC mRNA was decreased > 60% after a 2-day fast and was positively correlated with leptin mRNA. |
| 1132 | 9519731 | POMC mRNA was negatively correlated with both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) mRNA. |
| 1133 | 9519731 | Finally, treatment of both male and female ob/ob mice with leptin stimulated hypothalamic POMC mRNA by about threefold. |
| 1134 | 9519731 | These results suggest that impairment in production, processing, or responsiveness to alpha-MSH may be a common feature of obesity and that hypothalamic POMC neurons, stimulated by leptin, may constitute a link between leptin and the melanocortin system. |
| 1135 | 9519731 | Since alpha-MSH is coded for by the pro-opiomelanocortin (POMC) gene, we examined if POMC gene expression would be inhibited by fasting in normal mice or in models of obesity characterized by leptin insufficiency (ob/ob) or leptin insensitivity (db/db). |
| 1136 | 9519731 | In wild-type mice, hypothalamic POMC mRNA was decreased > 60% after a 2-day fast and was positively correlated with leptin mRNA. |
| 1137 | 9519731 | POMC mRNA was negatively correlated with both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) mRNA. |
| 1138 | 9519731 | Finally, treatment of both male and female ob/ob mice with leptin stimulated hypothalamic POMC mRNA by about threefold. |
| 1139 | 9519731 | These results suggest that impairment in production, processing, or responsiveness to alpha-MSH may be a common feature of obesity and that hypothalamic POMC neurons, stimulated by leptin, may constitute a link between leptin and the melanocortin system. |
| 1140 | 9519731 | Since alpha-MSH is coded for by the pro-opiomelanocortin (POMC) gene, we examined if POMC gene expression would be inhibited by fasting in normal mice or in models of obesity characterized by leptin insufficiency (ob/ob) or leptin insensitivity (db/db). |
| 1141 | 9519731 | In wild-type mice, hypothalamic POMC mRNA was decreased > 60% after a 2-day fast and was positively correlated with leptin mRNA. |
| 1142 | 9519731 | POMC mRNA was negatively correlated with both neuropeptide Y (NPY) and melanin-concentrating hormone (MCH) mRNA. |
| 1143 | 9519731 | Finally, treatment of both male and female ob/ob mice with leptin stimulated hypothalamic POMC mRNA by about threefold. |
| 1144 | 9519731 | These results suggest that impairment in production, processing, or responsiveness to alpha-MSH may be a common feature of obesity and that hypothalamic POMC neurons, stimulated by leptin, may constitute a link between leptin and the melanocortin system. |
| 1145 | 9566647 | The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). |
| 1146 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 1147 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 1148 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 1149 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 1150 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 1151 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 1152 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 1153 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 1154 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 1155 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 1156 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 1157 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 1158 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 1159 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 1160 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 1161 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 1162 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 1163 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 1164 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 1165 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 1166 | 9609982 | The serum prolactin, growth hormone, adrenocorticotropic hormone, and 11-deoxycortisol levels were elevated, but the estradiol and dehydroepiandrosterone-sulphate levels were within normal limits. |
| 1167 | 9610761 | Although insulin inhibited lipolysis induced by norepinephrine and ACTH at a concentration of 10(-10) M, it failed to inhibit basal lipolysis even at a concentration of 10(-6) M. |
| 1168 | 9610761 | These results indicate that insulin inhibits only the lipolysis induced by lipolytic agents such as norepinephrine and ACTH but not the basal lipolysis found in the absence of lipolytic agents. |
| 1169 | 9610761 | Although insulin inhibited lipolysis induced by norepinephrine and ACTH at a concentration of 10(-10) M, it failed to inhibit basal lipolysis even at a concentration of 10(-6) M. |
| 1170 | 9610761 | These results indicate that insulin inhibits only the lipolysis induced by lipolytic agents such as norepinephrine and ACTH but not the basal lipolysis found in the absence of lipolytic agents. |
| 1171 | 9667058 | The most relevant clinical aspects of hyperprolactinemia, acromegaly, Cushing's disease, secondary hyperthyroidism, syndrome of inappropriate ADH secretion, panhypopituitarism, growth hormone deficiency, gonadotropin deficiency, ACTH deficiency, TSH deficiency, and diabetes insipidus are discussed. |
| 1172 | 9743244 | ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. |
| 1173 | 9743244 | A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. |
| 1174 | 9743244 | In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/L) for 5 d. |
| 1175 | 9743244 | These results suggest that the increase in the CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. |
| 1176 | 9743244 | In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself. |
| 1177 | 9743244 | ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. |
| 1178 | 9743244 | A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. |
| 1179 | 9743244 | In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/L) for 5 d. |
| 1180 | 9743244 | These results suggest that the increase in the CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. |
| 1181 | 9743244 | In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself. |
| 1182 | 9743244 | ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. |
| 1183 | 9743244 | A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. |
| 1184 | 9743244 | In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/L) for 5 d. |
| 1185 | 9743244 | These results suggest that the increase in the CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. |
| 1186 | 9743244 | In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself. |
| 1187 | 9743244 | ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. |
| 1188 | 9743244 | A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. |
| 1189 | 9743244 | In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/L) for 5 d. |
| 1190 | 9743244 | These results suggest that the increase in the CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. |
| 1191 | 9743244 | In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself. |
| 1192 | 9743244 | ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. |
| 1193 | 9743244 | A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. |
| 1194 | 9743244 | In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/L) for 5 d. |
| 1195 | 9743244 | These results suggest that the increase in the CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. |
| 1196 | 9743244 | In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself. |
| 1197 | 9745408 | ACTH and cortisol responses to CRF, and PRL responses to TRH were normal in all cases, and LH and FSH responses to GnRH were compatible with pubertal stage. |
| 1198 | 9781630 | To test the hypothesis that the cortisol response to corticotropin (ACTH) infusion is independent of antecedent hypoglycemia, 10 healthy subjects received a standard ACTH infusion (0.25 mg Cosyntropin [Organon, West Orange, NJ] intravenously over 240 minutes) at 8:00 AM on day 1 and day 3 and a hypoglycemic insulin clamp study (1 mU/kg/min) at 8:00 AM on day 2. |
| 1199 | 9792536 | Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties. |
| 1200 | 9792536 | In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat. |
| 1201 | 9792536 | The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY. |
| 1202 | 9792536 | However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake. |
| 1203 | 9792536 | Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY. |
| 1204 | 9792536 | Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties. |
| 1205 | 9792536 | In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat. |
| 1206 | 9792536 | The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY. |
| 1207 | 9792536 | However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake. |
| 1208 | 9792536 | Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY. |
| 1209 | 9792536 | Among these, melanin-concentrating hormone (MCH) and neuropeptide Y (NPY) are potent appetite stimulants, whereas alpha-melanocyte-stimulating hormone (alpha-MSH), neurotensin, and glucagon-like peptide (GLP)-1(7-36) amide have appetite-suppressing properties. |
| 1210 | 9792536 | In the current study, we describe the functional interactions between orexigenic (appetite-stimulating: MCH and NPY) and anorectic (appetite-suppressing: alpha-MSH, neurotensin, and GLP-1) peptides after intracerebroventricular (i.c.v.) administration in the rat. |
| 1211 | 9792536 | The i.c.v. administration of GLP-1 completely prevents the orexigenic effects of both MCH and NPY. |
| 1212 | 9792536 | However, i.c.v. administration of alpha-MSH prevents only the orexigenic effect of MCH, as we have previously shown, but does not prevent the effect of NPY on food intake. |
| 1213 | 9792536 | Similarly, i.c.v. administration of neurotensin prevents only the orexigenic effect of MCH, but does not prevent the appetite-stimulating effect of NPY. |
| 1214 | 9794475 | In ob/ob mice, leptin deficiency results in increased expression of neuropeptide Y (NPY), agouti-related protein (AGRP), and melanin-concentrating hormone (MCH), and decreased expression of POMC. |
| 1215 | 9794475 | To define other potential sites of leptin resistance, we used in situ hybridization to evaluate the expression of messenger RNAs (mRNAs) encoding a number of peptides, including NPY, AGRP, MCH, and POMC. |
| 1216 | 9794475 | AGRP mRNA was also decreased, whereas POMC mRNA levels in the arcuate nucleus were the same as control. |
| 1217 | 9794475 | In ob/ob mice, leptin deficiency results in increased expression of neuropeptide Y (NPY), agouti-related protein (AGRP), and melanin-concentrating hormone (MCH), and decreased expression of POMC. |
| 1218 | 9794475 | To define other potential sites of leptin resistance, we used in situ hybridization to evaluate the expression of messenger RNAs (mRNAs) encoding a number of peptides, including NPY, AGRP, MCH, and POMC. |
| 1219 | 9794475 | AGRP mRNA was also decreased, whereas POMC mRNA levels in the arcuate nucleus were the same as control. |
| 1220 | 9794475 | In ob/ob mice, leptin deficiency results in increased expression of neuropeptide Y (NPY), agouti-related protein (AGRP), and melanin-concentrating hormone (MCH), and decreased expression of POMC. |
| 1221 | 9794475 | To define other potential sites of leptin resistance, we used in situ hybridization to evaluate the expression of messenger RNAs (mRNAs) encoding a number of peptides, including NPY, AGRP, MCH, and POMC. |
| 1222 | 9794475 | AGRP mRNA was also decreased, whereas POMC mRNA levels in the arcuate nucleus were the same as control. |
| 1223 | 9806554 | The peak on chromosome 2 coincided with the region containing the gene (POMC) encoding pro-opiomelanocortin, a locus previously linked to leptin levels and fat mass in a Mexican-American population and shown to be mutated in obese humans. |
| 1224 | 9807060 | To determine the effects of both corticosterone (B) and chronic stressors on acute ACTH responses to restraint, young male rats were exposed to streptozotocin-induced diabetes, cold (5-7 degreesC) or intracerebroventricular (icv) neuropeptide Y (NPY) for 5 d and then exposed to restraint within 2 h after lights on. |
| 1225 | 9807060 | By contrast, there was no ACTH or B response to restraint in NPY-infused intact rats. |
| 1226 | 9807060 | To determine the effects of both corticosterone (B) and chronic stressors on acute ACTH responses to restraint, young male rats were exposed to streptozotocin-induced diabetes, cold (5-7 degreesC) or intracerebroventricular (icv) neuropeptide Y (NPY) for 5 d and then exposed to restraint within 2 h after lights on. |
| 1227 | 9807060 | By contrast, there was no ACTH or B response to restraint in NPY-infused intact rats. |
| 1228 | 9819197 | The agouti-related protein gene (Agrp) is a novel gene implicated in the control of feeding behavior. |
| 1229 | 9819197 | The hypothalamic expression of Agrp is regulated by leptin, and overexpression of Agrp in transgenic animals results in obesity and diabetes. |
| 1230 | 9819197 | Both forms act as competitive antagonists of alpha-melanocyte stimulating hormone (alpha-MSH) at melanocortin-3 (MC-3) and melanocortin-4 receptors (MC-4). |
| 1231 | 9888542 | OB protein leptin inhibits the secretion of cortisol in primary cultures of bovine adrenocortical cells and down-regulates 17alpha-hydroxylase cytochrome P450 mRNA expression. |
| 1232 | 9888542 | To analyze if leptin regulates other major enzymes involved in adrenal steroidogenesis we tested its effect on mRNA expression for two further key enzymes, C21-hydroxylase (P450C21) and side-chain cleavage enzyme (P450SCC). |
| 1233 | 9888542 | Addition of leptin led to a reduction of ACTH-stimulated mRNA accumulation of 73% for P450C21 and of 45% for P450SCC. |
| 1234 | 10064107 | Plasma concentrations of insulin, glucagon and beta-endorphin- were also determined using radioimmunoassay. |
| 1235 | 10064107 | Thus we suggest that electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous beta-endorphin which reduces plasma glucose concentration in an insulin-dependent manner. |
| 1236 | 10064107 | Plasma concentrations of insulin, glucagon and beta-endorphin- were also determined using radioimmunoassay. |
| 1237 | 10064107 | Thus we suggest that electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous beta-endorphin which reduces plasma glucose concentration in an insulin-dependent manner. |
| 1238 | 10070149 | Rats were fasted overnight to promote feeding behavior, then injected intraperitoneally with LPS (100 micrograms/kg ip), followed 30 min later by intracerebroventricular injection of either alpha-MSH or the melanocortin receptor subtype 3/subtype 4 (MC3-R/MC4-R) antagonist SHU-9119. |
| 1239 | 10070149 | Central MC3-R/MC4-R blockade did not affect Tb or food intake in the absence of LPS treatment, but it reversed the LPS-induced reduction in 24-h food intake and increased LPS-induced fever without altering the LPS-induced suppression of locomotion. |
| 1240 | 10079035 | Expression of leptin receptor (OB-R) mRNA was detected in the human anterior pituitary as well as in ACTH-secreting and nonsecreting pituitary adenomas by RT-PCR with primers recognizing all receptor splice variants. |
| 1241 | 10099967 | Gonadotrophin releasing hormone (GnRH), corticotrophin releasing hormone (CRH), metoclopramide and thyroid releasing hormone (TRH) tests were performed in 15 diabetic women, eight amenorrhoeic (AD) and seven eumenorrhoeic (ED). |
| 1242 | 10099967 | The AD women had lower plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, oestradiol, androstenedione and 17-hydroxyprogesterone (17-OHP) than the ED women. |
| 1243 | 10099967 | The responses of pituitary gonadotrophins to GnRH, and of thyroid stimulating hormone (TSH) to TRH, were similar in both groups. |
| 1244 | 10099967 | The AD women had a lower prolactin response to TRH and metoclopramide, and lower ACTH and cortisol responses to CRH, than the ED women. |
| 1245 | 10208096 | The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m. cortisolemia, Aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, insulin hypoglycemia, etc.; inhibition tests: "overnight" and high dose dexamethasone. |
| 1246 | 10208096 | The Authors hypothesize that the ESS may be a "new" hypothalamic syndrome (compression/stretching on hypophysis and/or hypophyseal stalk by arachnoidocele; disorder of some hormones and neurotransmitters as leptin, neuropeptide Y, orexins, POMC-derived peptides, etc). |
| 1247 | 10208096 | The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m. cortisolemia, Aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, insulin hypoglycemia, etc.; inhibition tests: "overnight" and high dose dexamethasone. |
| 1248 | 10208096 | The Authors hypothesize that the ESS may be a "new" hypothalamic syndrome (compression/stretching on hypophysis and/or hypophyseal stalk by arachnoidocele; disorder of some hormones and neurotransmitters as leptin, neuropeptide Y, orexins, POMC-derived peptides, etc). |
| 1249 | 10233022 | STZ-induced diabetes decreases and insulin normalizes POMC mRNA in arcuate nucleus and pituitary in rats. |
| 1250 | 10233022 | Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. |
| 1251 | 10233022 | Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. |
| 1252 | 10233022 | Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A1-17 or beta-endorphin in paraventricular nucleus (PVN). alpha-Melanocyte-stimulating hormone (alpha-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. |
| 1253 | 10233022 | Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. |
| 1254 | 10233022 | In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. |
| 1255 | 10233022 | Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism. |
| 1256 | 10233022 | STZ-induced diabetes decreases and insulin normalizes POMC mRNA in arcuate nucleus and pituitary in rats. |
| 1257 | 10233022 | Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. |
| 1258 | 10233022 | Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. |
| 1259 | 10233022 | Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A1-17 or beta-endorphin in paraventricular nucleus (PVN). alpha-Melanocyte-stimulating hormone (alpha-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. |
| 1260 | 10233022 | Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. |
| 1261 | 10233022 | In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. |
| 1262 | 10233022 | Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism. |
| 1263 | 10233022 | STZ-induced diabetes decreases and insulin normalizes POMC mRNA in arcuate nucleus and pituitary in rats. |
| 1264 | 10233022 | Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. |
| 1265 | 10233022 | Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. |
| 1266 | 10233022 | Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A1-17 or beta-endorphin in paraventricular nucleus (PVN). alpha-Melanocyte-stimulating hormone (alpha-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. |
| 1267 | 10233022 | Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. |
| 1268 | 10233022 | In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. |
| 1269 | 10233022 | Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism. |
| 1270 | 10233022 | STZ-induced diabetes decreases and insulin normalizes POMC mRNA in arcuate nucleus and pituitary in rats. |
| 1271 | 10233022 | Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. |
| 1272 | 10233022 | Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. |
| 1273 | 10233022 | Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A1-17 or beta-endorphin in paraventricular nucleus (PVN). alpha-Melanocyte-stimulating hormone (alpha-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. |
| 1274 | 10233022 | Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. |
| 1275 | 10233022 | In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. |
| 1276 | 10233022 | Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism. |
| 1277 | 10233022 | STZ-induced diabetes decreases and insulin normalizes POMC mRNA in arcuate nucleus and pituitary in rats. |
| 1278 | 10233022 | Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. |
| 1279 | 10233022 | Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. |
| 1280 | 10233022 | Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A1-17 or beta-endorphin in paraventricular nucleus (PVN). alpha-Melanocyte-stimulating hormone (alpha-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. |
| 1281 | 10233022 | Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. |
| 1282 | 10233022 | In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. |
| 1283 | 10233022 | Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism. |
| 1284 | 10334300 | Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. |
| 1285 | 10334300 | We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. |
| 1286 | 10334300 | MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. |
| 1287 | 10334300 | We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. |
| 1288 | 10334300 | Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. |
| 1289 | 10334300 | This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. |
| 1290 | 10334300 | Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. |
| 1291 | 10334300 | We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. |
| 1292 | 10334300 | MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. |
| 1293 | 10334300 | We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. |
| 1294 | 10334300 | Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. |
| 1295 | 10334300 | This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. |
| 1296 | 10334300 | Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. |
| 1297 | 10334300 | We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. |
| 1298 | 10334300 | MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. |
| 1299 | 10334300 | We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. |
| 1300 | 10334300 | Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. |
| 1301 | 10334300 | This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. |
| 1302 | 10334300 | Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. |
| 1303 | 10334300 | We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. |
| 1304 | 10334300 | MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. |
| 1305 | 10334300 | We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. |
| 1306 | 10334300 | Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. |
| 1307 | 10334300 | This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. |
| 1308 | 10334300 | Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. |
| 1309 | 10334300 | We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. |
| 1310 | 10334300 | MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. |
| 1311 | 10334300 | We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. |
| 1312 | 10334300 | Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. |
| 1313 | 10334300 | This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. |
| 1314 | 10372707 | The roles of insulin sensitivity, insulin-like growth factor I (IGF-I), and IGF-binding protein-1 and -3 in the hyperandrogenism of African-American and Caribbean Hispanic girls with premature adrenarche. |
| 1315 | 10372707 | As insulin and insulin-like growth factors (IGFs) have been implicated in the pathogenesis of PCOS, we hypothesize that they may also have a role in the hyperandrogenism of premature adrenarche. |
| 1316 | 10372707 | Fasting levels of IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, sex hormone-binding globulin, and free testosterone (T) were also obtained. |
| 1317 | 10372707 | IGF-I correlated inversely with S(I) (r = -0.94; P < 0.001) and correlated directly with the ACTH-stimulated levels of 17OHPreg (r = 0.8; P < 0.001) and AS (r = 0.63; P < 0.05). |
| 1318 | 10372707 | IGF-I also correlated with the ACTH-stimulated ratios of 17OHPreg/17OHP (r = 0.61; P < 0.05), 17OHPreg/DHEA (r = 0.9; P < 0.001), 17OHP/AS (r = 0.79; P < 0.001), and DHEA/AS (r = 0.96; P < 0.001). |
| 1319 | 10372707 | IGFBP-1 correlated inversely with the ACTH-stimulated levels of 17OHPreg (r = -0.38; P < 0.05) and DHEA (r = -0.36; P < 0.05). |
| 1320 | 10372707 | There was a significant inverse correlation among ACTH-stimulated hormone levels, S(I), and IGFBP-1, whereas IGF-I correlated directly with ACTH-stimulated androgens. |
| 1321 | 10372707 | The roles of insulin sensitivity, insulin-like growth factor I (IGF-I), and IGF-binding protein-1 and -3 in the hyperandrogenism of African-American and Caribbean Hispanic girls with premature adrenarche. |
| 1322 | 10372707 | As insulin and insulin-like growth factors (IGFs) have been implicated in the pathogenesis of PCOS, we hypothesize that they may also have a role in the hyperandrogenism of premature adrenarche. |
| 1323 | 10372707 | Fasting levels of IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, sex hormone-binding globulin, and free testosterone (T) were also obtained. |
| 1324 | 10372707 | IGF-I correlated inversely with S(I) (r = -0.94; P < 0.001) and correlated directly with the ACTH-stimulated levels of 17OHPreg (r = 0.8; P < 0.001) and AS (r = 0.63; P < 0.05). |
| 1325 | 10372707 | IGF-I also correlated with the ACTH-stimulated ratios of 17OHPreg/17OHP (r = 0.61; P < 0.05), 17OHPreg/DHEA (r = 0.9; P < 0.001), 17OHP/AS (r = 0.79; P < 0.001), and DHEA/AS (r = 0.96; P < 0.001). |
| 1326 | 10372707 | IGFBP-1 correlated inversely with the ACTH-stimulated levels of 17OHPreg (r = -0.38; P < 0.05) and DHEA (r = -0.36; P < 0.05). |
| 1327 | 10372707 | There was a significant inverse correlation among ACTH-stimulated hormone levels, S(I), and IGFBP-1, whereas IGF-I correlated directly with ACTH-stimulated androgens. |
| 1328 | 10372707 | The roles of insulin sensitivity, insulin-like growth factor I (IGF-I), and IGF-binding protein-1 and -3 in the hyperandrogenism of African-American and Caribbean Hispanic girls with premature adrenarche. |
| 1329 | 10372707 | As insulin and insulin-like growth factors (IGFs) have been implicated in the pathogenesis of PCOS, we hypothesize that they may also have a role in the hyperandrogenism of premature adrenarche. |
| 1330 | 10372707 | Fasting levels of IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, sex hormone-binding globulin, and free testosterone (T) were also obtained. |
| 1331 | 10372707 | IGF-I correlated inversely with S(I) (r = -0.94; P < 0.001) and correlated directly with the ACTH-stimulated levels of 17OHPreg (r = 0.8; P < 0.001) and AS (r = 0.63; P < 0.05). |
| 1332 | 10372707 | IGF-I also correlated with the ACTH-stimulated ratios of 17OHPreg/17OHP (r = 0.61; P < 0.05), 17OHPreg/DHEA (r = 0.9; P < 0.001), 17OHP/AS (r = 0.79; P < 0.001), and DHEA/AS (r = 0.96; P < 0.001). |
| 1333 | 10372707 | IGFBP-1 correlated inversely with the ACTH-stimulated levels of 17OHPreg (r = -0.38; P < 0.05) and DHEA (r = -0.36; P < 0.05). |
| 1334 | 10372707 | There was a significant inverse correlation among ACTH-stimulated hormone levels, S(I), and IGFBP-1, whereas IGF-I correlated directly with ACTH-stimulated androgens. |
| 1335 | 10372707 | The roles of insulin sensitivity, insulin-like growth factor I (IGF-I), and IGF-binding protein-1 and -3 in the hyperandrogenism of African-American and Caribbean Hispanic girls with premature adrenarche. |
| 1336 | 10372707 | As insulin and insulin-like growth factors (IGFs) have been implicated in the pathogenesis of PCOS, we hypothesize that they may also have a role in the hyperandrogenism of premature adrenarche. |
| 1337 | 10372707 | Fasting levels of IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, sex hormone-binding globulin, and free testosterone (T) were also obtained. |
| 1338 | 10372707 | IGF-I correlated inversely with S(I) (r = -0.94; P < 0.001) and correlated directly with the ACTH-stimulated levels of 17OHPreg (r = 0.8; P < 0.001) and AS (r = 0.63; P < 0.05). |
| 1339 | 10372707 | IGF-I also correlated with the ACTH-stimulated ratios of 17OHPreg/17OHP (r = 0.61; P < 0.05), 17OHPreg/DHEA (r = 0.9; P < 0.001), 17OHP/AS (r = 0.79; P < 0.001), and DHEA/AS (r = 0.96; P < 0.001). |
| 1340 | 10372707 | IGFBP-1 correlated inversely with the ACTH-stimulated levels of 17OHPreg (r = -0.38; P < 0.05) and DHEA (r = -0.36; P < 0.05). |
| 1341 | 10372707 | There was a significant inverse correlation among ACTH-stimulated hormone levels, S(I), and IGFBP-1, whereas IGF-I correlated directly with ACTH-stimulated androgens. |
| 1342 | 10395233 | The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin D (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. |
| 1343 | 10436815 | Pancreatic endocrine tumors (PET's) can be divided on a clinical and pathologic basis into ten classes [insulinomas, gastrinomas (Zollinger-Ellison syndrome), VIPomas (Verner-Morrison syndrome, WDHA, pancreatic cholera), glucagonomas, somatostatinomas, ACTH-releasing tumors (ACTHomas), growth hormone-releasing factor secreting tumors (GRFomas), nonfunctioning or pancreatic polypeptide secreting tumors (non-functioning PET), PET's causing carcinoid syndrome and PET's causing hypercalcemia)]. |
| 1344 | 10480603 | The effects of corticotropin-releasing factor (CRF) on the intracellular concentration of Ca2+ were studied in isolated single beta-cells of the rat islet. |
| 1345 | 10480603 | Immunohistochemical staining using CRF-receptor antibodies revealed the presence of both type 1 (CRF-R1) and type 2 (CRF-R2) receptors for CRF in the majority of islet cells. |
| 1346 | 10480603 | These results suggest that in single beta-cells of rat islets, CRF, through its own receptor, potentiates Ca2+ influx through the L-type Ca2+ channel by activation of the cAMP/protein kinase A signaling pathway. |
| 1347 | 10499510 | Fasting regulates hypothalamic neuropeptide Y, agouti-related peptide, and proopiomelanocortin in diabetic mice independent of changes in leptin or insulin. |
| 1348 | 10499510 | Fasting increases hypothalamic neuropeptide Y (NPY) and agouti-related peptide (AGRP) messenger RNA (mRNA) and reduces hypothalamic POMC mRNA, and is also characterized by a reduction in plasma leptin, insulin, and glucose, each of which has been implicated in the regulation of hypothalamic gene expression. |
| 1349 | 10499510 | To further evaluate the roles of leptin, insulin, and glucose in mediating effects of fasting, we examined hypothalamic gene expression in nondiabetic and streptozotocin (STZ)-induced diabetic mice both under ad lib fed and 48-h fasted conditions. |
| 1350 | 10499510 | In both diabetic and nondiabetic mice, fasting stimulated hypothalamic NPY and AGRP mRNA and inhibited hypothalamic POMC mRNA and adipose leptin mRNA. |
| 1351 | 10499510 | However, in diabetic mice fasting had no effect on plasma leptin and insulin while decreasing plasma glucose, whereas in nondiabetic mice fasting decreased plasma leptin, insulin, and glucose. |
| 1352 | 10499510 | Furthermore, in nondiabetic fasted mice, NPY and AGRP mRNA were higher, and POMC mRNA and plasma glucose were lower, than in diabetic ad lib fed mice, even though insulin and leptin were similar in these two groups. |
| 1353 | 10499510 | These data are consistent with the hypothesis that although leptin and insulin regulate hypothalamic gene expression, glucose or other factors may have independent effects on hypothalamic and adipose gene expression under conditions of low insulin and leptin. |
| 1354 | 10499510 | Fasting regulates hypothalamic neuropeptide Y, agouti-related peptide, and proopiomelanocortin in diabetic mice independent of changes in leptin or insulin. |
| 1355 | 10499510 | Fasting increases hypothalamic neuropeptide Y (NPY) and agouti-related peptide (AGRP) messenger RNA (mRNA) and reduces hypothalamic POMC mRNA, and is also characterized by a reduction in plasma leptin, insulin, and glucose, each of which has been implicated in the regulation of hypothalamic gene expression. |
| 1356 | 10499510 | To further evaluate the roles of leptin, insulin, and glucose in mediating effects of fasting, we examined hypothalamic gene expression in nondiabetic and streptozotocin (STZ)-induced diabetic mice both under ad lib fed and 48-h fasted conditions. |
| 1357 | 10499510 | In both diabetic and nondiabetic mice, fasting stimulated hypothalamic NPY and AGRP mRNA and inhibited hypothalamic POMC mRNA and adipose leptin mRNA. |
| 1358 | 10499510 | However, in diabetic mice fasting had no effect on plasma leptin and insulin while decreasing plasma glucose, whereas in nondiabetic mice fasting decreased plasma leptin, insulin, and glucose. |
| 1359 | 10499510 | Furthermore, in nondiabetic fasted mice, NPY and AGRP mRNA were higher, and POMC mRNA and plasma glucose were lower, than in diabetic ad lib fed mice, even though insulin and leptin were similar in these two groups. |
| 1360 | 10499510 | These data are consistent with the hypothesis that although leptin and insulin regulate hypothalamic gene expression, glucose or other factors may have independent effects on hypothalamic and adipose gene expression under conditions of low insulin and leptin. |
| 1361 | 10499510 | Fasting regulates hypothalamic neuropeptide Y, agouti-related peptide, and proopiomelanocortin in diabetic mice independent of changes in leptin or insulin. |
| 1362 | 10499510 | Fasting increases hypothalamic neuropeptide Y (NPY) and agouti-related peptide (AGRP) messenger RNA (mRNA) and reduces hypothalamic POMC mRNA, and is also characterized by a reduction in plasma leptin, insulin, and glucose, each of which has been implicated in the regulation of hypothalamic gene expression. |
| 1363 | 10499510 | To further evaluate the roles of leptin, insulin, and glucose in mediating effects of fasting, we examined hypothalamic gene expression in nondiabetic and streptozotocin (STZ)-induced diabetic mice both under ad lib fed and 48-h fasted conditions. |
| 1364 | 10499510 | In both diabetic and nondiabetic mice, fasting stimulated hypothalamic NPY and AGRP mRNA and inhibited hypothalamic POMC mRNA and adipose leptin mRNA. |
| 1365 | 10499510 | However, in diabetic mice fasting had no effect on plasma leptin and insulin while decreasing plasma glucose, whereas in nondiabetic mice fasting decreased plasma leptin, insulin, and glucose. |
| 1366 | 10499510 | Furthermore, in nondiabetic fasted mice, NPY and AGRP mRNA were higher, and POMC mRNA and plasma glucose were lower, than in diabetic ad lib fed mice, even though insulin and leptin were similar in these two groups. |
| 1367 | 10499510 | These data are consistent with the hypothesis that although leptin and insulin regulate hypothalamic gene expression, glucose or other factors may have independent effects on hypothalamic and adipose gene expression under conditions of low insulin and leptin. |
| 1368 | 10499510 | Fasting regulates hypothalamic neuropeptide Y, agouti-related peptide, and proopiomelanocortin in diabetic mice independent of changes in leptin or insulin. |
| 1369 | 10499510 | Fasting increases hypothalamic neuropeptide Y (NPY) and agouti-related peptide (AGRP) messenger RNA (mRNA) and reduces hypothalamic POMC mRNA, and is also characterized by a reduction in plasma leptin, insulin, and glucose, each of which has been implicated in the regulation of hypothalamic gene expression. |
| 1370 | 10499510 | To further evaluate the roles of leptin, insulin, and glucose in mediating effects of fasting, we examined hypothalamic gene expression in nondiabetic and streptozotocin (STZ)-induced diabetic mice both under ad lib fed and 48-h fasted conditions. |
| 1371 | 10499510 | In both diabetic and nondiabetic mice, fasting stimulated hypothalamic NPY and AGRP mRNA and inhibited hypothalamic POMC mRNA and adipose leptin mRNA. |
| 1372 | 10499510 | However, in diabetic mice fasting had no effect on plasma leptin and insulin while decreasing plasma glucose, whereas in nondiabetic mice fasting decreased plasma leptin, insulin, and glucose. |
| 1373 | 10499510 | Furthermore, in nondiabetic fasted mice, NPY and AGRP mRNA were higher, and POMC mRNA and plasma glucose were lower, than in diabetic ad lib fed mice, even though insulin and leptin were similar in these two groups. |
| 1374 | 10499510 | These data are consistent with the hypothesis that although leptin and insulin regulate hypothalamic gene expression, glucose or other factors may have independent effects on hypothalamic and adipose gene expression under conditions of low insulin and leptin. |
| 1375 | 10512369 | Involvement of agouti-related protein, an endogenous antagonist of hypothalamic melanocortin receptor, in leptin action. |
| 1376 | 10512369 | To understand the role of agouti-related protein (AGRP), an endogenous antagonist of hypothalamic melanocortin receptor, in leptin action, we produced a full-length recombinant AGRP and examined its effect on the satiety effect of leptin. |
| 1377 | 10512369 | We also studied leptin's regulation of hypothalamic AGRP mRNA expression. |
| 1378 | 10512369 | The leptin-induced inhibition of food intake and body weight was reversed by co-injection of AGRP in a dose-dependent manner. |
| 1379 | 10512369 | Hypothalamic AGRP mRNA expression was upregulated in leptin-deficient ob/ob mice and leptin receptor-deficient db/db mice and downregulated in lethal yellow agouti mice (KKAy mice) with hyperleptinemia. |
| 1380 | 10512369 | A single i.c.v. injection of leptin reversed the increased AGRP mRNA levels in ob/ob mice but not in db/db mice. |
| 1381 | 10512369 | In control mice and KKAy mice, AGRP mRNA expression was upregulated during fasting, when plasma leptin concentrations were decreased. |
| 1382 | 10512369 | This study provides the first direct evidence that AGRP is a negative regulator of leptin action, and leptin downregulates hypothalamic AGRP production. |
| 1383 | 10512369 | Because leptin is shown to increase hypothalamic alpha-melanocyte stimulating hormone (alpha-MSH) production, our data suggest that its action via the hypothalamic melanocortin system is determined by the balance between the levels of its agonist and antagonist, alpha-MSH and AGRP. |
| 1384 | 10563747 | Responses of plasma gonadotropin and corticotropin-cortisol levels to respective hypothalamic hormones were delayed or blunted, but the response of plasma prolactin to thyrotropin-releasing hormone was exaggerated. |
| 1385 | 10583426 | Finally, by crossing the blood-brain barrier insulin exerts a host a central effects (sympatho-excitation, vagal withdrawal, stimulation of corticotropin releasing factor), collectively resembling a stress reaction. |
| 1386 | 10596369 | Panhypopituitarism was diagnosed after measuring the basal hormone levels (ACTH, TSH, FT3, FT4, Cortisol, Prolactin, LH, FSH, ADH) and conducting the pituitary stimulation test. |
| 1387 | 10596369 | The present case report is the first description of a viral infection on of the central nervous system (CNS) in combination with parkinsonism, diabetes insipidus, persistent panhypopituitarism and hyperprolactinemia. |
| 1388 | 10604121 | The Cushing's syndrome diagnosis due to rare ectopic neuroendocrine tumour adrenocorticotropic hormone secretion can be made only with selective angiography, whereas non-functional and pancreatic polypeptide producing neuroendocrine tumours (PPoma) present without any symptoms. |
| 1389 | 10606438 | An accumulation of evidence implicates leptin, insulin, glucocorticoids, proopiomelanocortin (POMC), and neuropeptide Y (NPY) interactions as being integral to metabolic control associated with neuroendocrine-endocrine functioning. |
| 1390 | 10626548 | African-American and Caribbean-Hispanic girls with premature adrenarche are frequently obese with marked hyperandrogenism, signs which correlate with the degree of insulin resistance (i.e., those girls who are obese and insulin resistant tend to have higher levels of adrenocorticotropic hormone-stimulated androgens). |
| 1391 | 10640899 | ACTH receptor gene analysis revealed no mutations in the ACTH receptor-coding region. |
| 1392 | 10657511 | Neuropeptide Y (NPY), melanin concentrating hormone (MCH), orexins A and B, galanin, and agouti -related peptide (AgRP) all act to stimulate feeding while alpha-melanocyte stimulating hormone (alphaMSH), corticotropin releasing hormone (CRH), cholecystokinin (CCK), cocaine and amphetamine regulated transcript (CART), neurotensin, glucagon-like peptide 1 (GLP 1), and bombesin have anorectic actions.(1) Leptin, expressed in the periphery in white adipose tissue, acts in the CNS to modulate the expression of several of these hypothalamic peptides.(1) This creates a functional link between the adipose tissue and the brain that translates the information on body fat provided by leptin to input into energy balance regulating processes. |
| 1393 | 10657511 | In the current review we examine the significant role of the melanocortin system (alphaMSH, agouti and AgRP peptides, and their receptors and mahogany protein) and melanin concentrating hormone in the regulation of energy balance. |
| 1394 | 10661502 | In addition, we examined ACTH secretion following CRF administration in vivo and in vitro to characterize the mechanisms regulating the HPA axis in OLETF rats. |
| 1395 | 10661502 | Plasma ACTH levels following CRF (2 microg/kg, i.v.) in OLETF and LETO rats showed statistically significant increases at 10 and 30 min after CRF administration compared to ACTH levels at 0 min, however, the peak plasma ACTH level in OLETF rats at 10 min after CRF administration was significantly greater than in LETO rats. |
| 1396 | 10661502 | CRF (10 ng/ml) significantly increased ACTH secretion in pituitary cultures from OLETF compared to LETO rats. |
| 1397 | 10661502 | In addition, we examined ACTH secretion following CRF administration in vivo and in vitro to characterize the mechanisms regulating the HPA axis in OLETF rats. |
| 1398 | 10661502 | Plasma ACTH levels following CRF (2 microg/kg, i.v.) in OLETF and LETO rats showed statistically significant increases at 10 and 30 min after CRF administration compared to ACTH levels at 0 min, however, the peak plasma ACTH level in OLETF rats at 10 min after CRF administration was significantly greater than in LETO rats. |
| 1399 | 10661502 | CRF (10 ng/ml) significantly increased ACTH secretion in pituitary cultures from OLETF compared to LETO rats. |
| 1400 | 10661502 | In addition, we examined ACTH secretion following CRF administration in vivo and in vitro to characterize the mechanisms regulating the HPA axis in OLETF rats. |
| 1401 | 10661502 | Plasma ACTH levels following CRF (2 microg/kg, i.v.) in OLETF and LETO rats showed statistically significant increases at 10 and 30 min after CRF administration compared to ACTH levels at 0 min, however, the peak plasma ACTH level in OLETF rats at 10 min after CRF administration was significantly greater than in LETO rats. |
| 1402 | 10661502 | CRF (10 ng/ml) significantly increased ACTH secretion in pituitary cultures from OLETF compared to LETO rats. |
| 1403 | 10671817 | Basal levels of adrenocorticotropic hormone, cortisol, growth hormone, insulin-like growth factor-I, prolactin, glucagon, estradiol, progesterone, human placental lactogen and human chorionic gonadotropin were investigated in 15 nonobese women with GDM and 26 matched normal pregnant women (N). |
| 1404 | 10754162 | Adrenocorticotropic hormone-independent macronodular adrenal hyperplasia (AIMAH) was endocrinologically and histopathologically diagnosed. |
| 1405 | 10768826 | Natriuretic peptides (ANP, BNP and CNP) comprise a family of structurally related peptides, which are derived from three different genes and which share a 17-amino acid internal ring. |
| 1406 | 10768826 | Besides their peripheral involvement in diuresis and blood pressure regulation these peptides, their bioactive fragments and their corresponding receptors (natriuretic peptide receptors NPR-A, NPR-B and NPR-C) are found throughout the central nervous system (CNS): NPR-A and NPR-C are found on neurons and astrocytes, while NPR-B is located mainly on neurons and partially colocalizes with NPR-A. |
| 1407 | 10768826 | In the CNS of man and rodents NPR-A is found mainly in cortex and hippocampus, whereas NPR-B is present in the amygdala and several brainstem regulatory sites. |
| 1408 | 10768826 | Natriuretic peptides are specifically involved in the regulation of the hypothalamo-pituitary-adrenocortical (HPA) system: in man and rodents ANP inhibits the HPA system at all regulatory levels, while CNP stimulates the release of cortisol. |
| 1409 | 10768826 | Complementarily, the anatomic structure of natriuretic peptide systems within the CNS supports an important role for these in normal and pathologic emotional behaviour (e.g. anxiety and panic): in rodents ANP was found to reduce anxiety levels, whereas CNP induced the opposite effect. |
| 1410 | 10768826 | Moreover, panic anxiety and concomitant ACTH and cortisol secretion elicited by stimulation with the panicogen cholecystokinin-tetrapeptide were also attenuated by ANP infusions in patients as well as in healthy volunteers. |
| 1411 | 10768834 | This study was designed to analyze the sequence and the expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas. |
| 1412 | 10768834 | However, using a semiquantitative PCR approach coamplifying the house-keeping gene GAPDH we detected a reduced expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas when compared with normal pituitaries. |
| 1413 | 10768834 | We suggest that the decreased CRF-BP gene expression in ACTH-secreting pituitary adenomas is most likely an effect due to high cortisol levels in Cushing patients. |
| 1414 | 10768834 | This study was designed to analyze the sequence and the expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas. |
| 1415 | 10768834 | However, using a semiquantitative PCR approach coamplifying the house-keeping gene GAPDH we detected a reduced expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas when compared with normal pituitaries. |
| 1416 | 10768834 | We suggest that the decreased CRF-BP gene expression in ACTH-secreting pituitary adenomas is most likely an effect due to high cortisol levels in Cushing patients. |
| 1417 | 10768834 | This study was designed to analyze the sequence and the expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas. |
| 1418 | 10768834 | However, using a semiquantitative PCR approach coamplifying the house-keeping gene GAPDH we detected a reduced expression of CRF-BP mRNA in ACTH-secreting pituitary adenomas when compared with normal pituitaries. |
| 1419 | 10768834 | We suggest that the decreased CRF-BP gene expression in ACTH-secreting pituitary adenomas is most likely an effect due to high cortisol levels in Cushing patients. |
| 1420 | 10800764 | Multiple pituitary hormone hypersecretions have been already described, but the combination of PRL and ACTH excess is rare. |
| 1421 | 10800764 | The patient reported seems atypical for the following reasons: 1) the concomitant PRL and ACTH hypersecretions; 2) the clinical presentation with hypercortisolism following hyperprolactinemia; 3) the surgical cure of hypercortisolism with persisting hyperprolactinemia. |
| 1422 | 10800764 | Multiple pituitary hormone hypersecretions have been already described, but the combination of PRL and ACTH excess is rare. |
| 1423 | 10800764 | The patient reported seems atypical for the following reasons: 1) the concomitant PRL and ACTH hypersecretions; 2) the clinical presentation with hypercortisolism following hyperprolactinemia; 3) the surgical cure of hypercortisolism with persisting hyperprolactinemia. |
| 1424 | 10816641 | Emphasis on PC1, PC2/7B2, POMC and the novel enzyme SKI-1. |
| 1425 | 10816641 | Processing of POMC at dibasic residues is tissue-specific and is performed by either PC1 alone (resulting in ACTH and beta LPH, anterior pituitary corticotrophes) or by a combination of PC1 and PC2 (yielding alpha MSH and beta END, pituitary neurointermediate lobe and hypothalamus). |
| 1426 | 10816641 | Structure-function studies of these enzymes demonstrated the presence of N- and C-terminal domains, as well as specific amino acids within the catalytic segment that influence the degree of activity of each enzyme and the interaction of PC2 with 7B2. |
| 1427 | 10816641 | The phenotypic consequences of the absence of genetic expression of either PC1 or PC2 are now explored using knockout mice and in human patients suffering from obesity and diabetes. |
| 1428 | 10816641 | Emphasis on PC1, PC2/7B2, POMC and the novel enzyme SKI-1. |
| 1429 | 10816641 | Processing of POMC at dibasic residues is tissue-specific and is performed by either PC1 alone (resulting in ACTH and beta LPH, anterior pituitary corticotrophes) or by a combination of PC1 and PC2 (yielding alpha MSH and beta END, pituitary neurointermediate lobe and hypothalamus). |
| 1430 | 10816641 | Structure-function studies of these enzymes demonstrated the presence of N- and C-terminal domains, as well as specific amino acids within the catalytic segment that influence the degree of activity of each enzyme and the interaction of PC2 with 7B2. |
| 1431 | 10816641 | The phenotypic consequences of the absence of genetic expression of either PC1 or PC2 are now explored using knockout mice and in human patients suffering from obesity and diabetes. |
| 1432 | 10822340 | Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes. |
| 1433 | 10822340 | Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR. |
| 1434 | 10822340 | ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR. |
| 1435 | 10822340 | CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland. |
| 1436 | 10822340 | This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans. |
| 1437 | 10822340 | Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes. |
| 1438 | 10822340 | Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR. |
| 1439 | 10822340 | ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR. |
| 1440 | 10822340 | CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland. |
| 1441 | 10822340 | This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans. |
| 1442 | 10822340 | Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes. |
| 1443 | 10822340 | Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR. |
| 1444 | 10822340 | ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR. |
| 1445 | 10822340 | CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland. |
| 1446 | 10822340 | This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans. |
| 1447 | 10822340 | Treatment of rats or monkeys with the novel CRH receptor type 1 (CRH-R1) antagonist antalarmin inhibits the HPA and/or the SA/SS axes. |
| 1448 | 10822340 | Expression of CRH, ACTH, CRH type I and type II receptor mRNA were analyzed by reverse-transcription (RT) PCR. |
| 1449 | 10822340 | ACTH, CRH, and CRH-R1 and CRH-R2 mRNAs were expressed in the human adrenal as determined by RT-PCR. |
| 1450 | 10822340 | CRH, ACTH, and both CRH-R1 and CRH-R2 mRNAs are expressed in the adult human adrenal gland. |
| 1451 | 10822340 | This effect is blocked by antalarmin, a selective CRH-R1 receptor antagonist, suggesting that CRH-R1 receptors are involved in an intraadrenal CRH/ACTH control system in humans. |
| 1452 | 10868932 | We investigated which hypothalamic areas known to express MC4R are involved in the regulation of feeding by using alpha-melanocyte-stimulating hormone (alpha-MSH), an endogenous MC4R agonist, and agouti-related peptide (Agrp), an endogenous MC4R antagonist. |
| 1453 | 10868932 | Agrp (83-132) (0.1 nmol) and [Nle4, D-Phe7]alpha(-MSH (NDP-MSH) (0.1 nmol), a stable alpha-MSH analog, were administered to fed and fasted rats, respectively. |
| 1454 | 10868932 | The PVN, DMN, and MPO were the areas with the greatest response to Agrp and NDP-MSH. |
| 1455 | 10868932 | This study indicates that the hypothalamic nuclei expressing MC4R vary in their sensitivity to Agrp and alpha-MSH with regard to their effect on feeding. |
| 1456 | 10868932 | We investigated which hypothalamic areas known to express MC4R are involved in the regulation of feeding by using alpha-melanocyte-stimulating hormone (alpha-MSH), an endogenous MC4R agonist, and agouti-related peptide (Agrp), an endogenous MC4R antagonist. |
| 1457 | 10868932 | Agrp (83-132) (0.1 nmol) and [Nle4, D-Phe7]alpha(-MSH (NDP-MSH) (0.1 nmol), a stable alpha-MSH analog, were administered to fed and fasted rats, respectively. |
| 1458 | 10868932 | The PVN, DMN, and MPO were the areas with the greatest response to Agrp and NDP-MSH. |
| 1459 | 10868932 | This study indicates that the hypothalamic nuclei expressing MC4R vary in their sensitivity to Agrp and alpha-MSH with regard to their effect on feeding. |
| 1460 | 10868932 | We investigated which hypothalamic areas known to express MC4R are involved in the regulation of feeding by using alpha-melanocyte-stimulating hormone (alpha-MSH), an endogenous MC4R agonist, and agouti-related peptide (Agrp), an endogenous MC4R antagonist. |
| 1461 | 10868932 | Agrp (83-132) (0.1 nmol) and [Nle4, D-Phe7]alpha(-MSH (NDP-MSH) (0.1 nmol), a stable alpha-MSH analog, were administered to fed and fasted rats, respectively. |
| 1462 | 10868932 | The PVN, DMN, and MPO were the areas with the greatest response to Agrp and NDP-MSH. |
| 1463 | 10868932 | This study indicates that the hypothalamic nuclei expressing MC4R vary in their sensitivity to Agrp and alpha-MSH with regard to their effect on feeding. |
| 1464 | 10868941 | Effects of streptozotocin-induced diabetes and insulin treatment on the hypothalamic melanocortin system and muscle uncoupling protein 3 expression in rats. |
| 1465 | 10868941 | Agonists for melanocortin 4 (MC-4) receptors such as alpha-melanocyte-stimulating hormone (alpha-MSH), a product of proopiomelanocortin (POMC), reduce food intake, whereas hypothalamic agouti-related protein (AgRP) is a MC-4 receptor antagonist that increases food intake. |
| 1466 | 10868941 | Plasma leptin was markedly reduced in STZ diabetic rats (0.4 +/- 0.1 ng/ml; P < 0.005) compared with controls (3.0 +/- 0.4 ng/ml), an effect that was also partially reversed by insulin treatment (1.8 +/- 0.3 ng/ml). |
| 1467 | 10868941 | In untreated diabetic rats, hypothalamic POMC mRNA expression (measured by in situ hybridization) was reduced by 80% (P < 0.005), whereas AgRP mRNA levels were increased by 60% (P < 0.01), suggesting a marked decrease of hypothalamic melanocortin signaling. |
| 1468 | 10868941 | The change in POMC, but not in AgRP, mRNA levels was partially reversed by insulin treatment. |
| 1469 | 10868941 | By comparison, the effects of diabetes to increase hypothalamic neuropeptide Y (NPY) expression and to decrease corticotropin-releasing hormone (CRH) expression were normalized by insulin treatment, whereas the expression of mRNA encoding the long form of the leptin receptor in the arcuate nucleus was unaltered by diabetes or insulin treatment. |
| 1470 | 10868941 | UCP-3 mRNA expression in gastrocnemius muscle from diabetic rats was increased fourfold (P < 0.005), and the increase was prevented by insulin treatment. |
| 1471 | 10868941 | The effect of uncontrolled diabetes to decrease POMC, while increasing AgRP gene expression, suggests that reduced hypothalamic melanocortin signaling, along with increased NPY and decreased CRH signaling, could contribute to diabetic hyperphagia. |
| 1472 | 10868941 | Effects of streptozotocin-induced diabetes and insulin treatment on the hypothalamic melanocortin system and muscle uncoupling protein 3 expression in rats. |
| 1473 | 10868941 | Agonists for melanocortin 4 (MC-4) receptors such as alpha-melanocyte-stimulating hormone (alpha-MSH), a product of proopiomelanocortin (POMC), reduce food intake, whereas hypothalamic agouti-related protein (AgRP) is a MC-4 receptor antagonist that increases food intake. |
| 1474 | 10868941 | Plasma leptin was markedly reduced in STZ diabetic rats (0.4 +/- 0.1 ng/ml; P < 0.005) compared with controls (3.0 +/- 0.4 ng/ml), an effect that was also partially reversed by insulin treatment (1.8 +/- 0.3 ng/ml). |
| 1475 | 10868941 | In untreated diabetic rats, hypothalamic POMC mRNA expression (measured by in situ hybridization) was reduced by 80% (P < 0.005), whereas AgRP mRNA levels were increased by 60% (P < 0.01), suggesting a marked decrease of hypothalamic melanocortin signaling. |
| 1476 | 10868941 | The change in POMC, but not in AgRP, mRNA levels was partially reversed by insulin treatment. |
| 1477 | 10868941 | By comparison, the effects of diabetes to increase hypothalamic neuropeptide Y (NPY) expression and to decrease corticotropin-releasing hormone (CRH) expression were normalized by insulin treatment, whereas the expression of mRNA encoding the long form of the leptin receptor in the arcuate nucleus was unaltered by diabetes or insulin treatment. |
| 1478 | 10868941 | UCP-3 mRNA expression in gastrocnemius muscle from diabetic rats was increased fourfold (P < 0.005), and the increase was prevented by insulin treatment. |
| 1479 | 10868941 | The effect of uncontrolled diabetes to decrease POMC, while increasing AgRP gene expression, suggests that reduced hypothalamic melanocortin signaling, along with increased NPY and decreased CRH signaling, could contribute to diabetic hyperphagia. |
| 1480 | 10868941 | Effects of streptozotocin-induced diabetes and insulin treatment on the hypothalamic melanocortin system and muscle uncoupling protein 3 expression in rats. |
| 1481 | 10868941 | Agonists for melanocortin 4 (MC-4) receptors such as alpha-melanocyte-stimulating hormone (alpha-MSH), a product of proopiomelanocortin (POMC), reduce food intake, whereas hypothalamic agouti-related protein (AgRP) is a MC-4 receptor antagonist that increases food intake. |
| 1482 | 10868941 | Plasma leptin was markedly reduced in STZ diabetic rats (0.4 +/- 0.1 ng/ml; P < 0.005) compared with controls (3.0 +/- 0.4 ng/ml), an effect that was also partially reversed by insulin treatment (1.8 +/- 0.3 ng/ml). |
| 1483 | 10868941 | In untreated diabetic rats, hypothalamic POMC mRNA expression (measured by in situ hybridization) was reduced by 80% (P < 0.005), whereas AgRP mRNA levels were increased by 60% (P < 0.01), suggesting a marked decrease of hypothalamic melanocortin signaling. |
| 1484 | 10868941 | The change in POMC, but not in AgRP, mRNA levels was partially reversed by insulin treatment. |
| 1485 | 10868941 | By comparison, the effects of diabetes to increase hypothalamic neuropeptide Y (NPY) expression and to decrease corticotropin-releasing hormone (CRH) expression were normalized by insulin treatment, whereas the expression of mRNA encoding the long form of the leptin receptor in the arcuate nucleus was unaltered by diabetes or insulin treatment. |
| 1486 | 10868941 | UCP-3 mRNA expression in gastrocnemius muscle from diabetic rats was increased fourfold (P < 0.005), and the increase was prevented by insulin treatment. |
| 1487 | 10868941 | The effect of uncontrolled diabetes to decrease POMC, while increasing AgRP gene expression, suggests that reduced hypothalamic melanocortin signaling, along with increased NPY and decreased CRH signaling, could contribute to diabetic hyperphagia. |
| 1488 | 10868941 | Effects of streptozotocin-induced diabetes and insulin treatment on the hypothalamic melanocortin system and muscle uncoupling protein 3 expression in rats. |
| 1489 | 10868941 | Agonists for melanocortin 4 (MC-4) receptors such as alpha-melanocyte-stimulating hormone (alpha-MSH), a product of proopiomelanocortin (POMC), reduce food intake, whereas hypothalamic agouti-related protein (AgRP) is a MC-4 receptor antagonist that increases food intake. |
| 1490 | 10868941 | Plasma leptin was markedly reduced in STZ diabetic rats (0.4 +/- 0.1 ng/ml; P < 0.005) compared with controls (3.0 +/- 0.4 ng/ml), an effect that was also partially reversed by insulin treatment (1.8 +/- 0.3 ng/ml). |
| 1491 | 10868941 | In untreated diabetic rats, hypothalamic POMC mRNA expression (measured by in situ hybridization) was reduced by 80% (P < 0.005), whereas AgRP mRNA levels were increased by 60% (P < 0.01), suggesting a marked decrease of hypothalamic melanocortin signaling. |
| 1492 | 10868941 | The change in POMC, but not in AgRP, mRNA levels was partially reversed by insulin treatment. |
| 1493 | 10868941 | By comparison, the effects of diabetes to increase hypothalamic neuropeptide Y (NPY) expression and to decrease corticotropin-releasing hormone (CRH) expression were normalized by insulin treatment, whereas the expression of mRNA encoding the long form of the leptin receptor in the arcuate nucleus was unaltered by diabetes or insulin treatment. |
| 1494 | 10868941 | UCP-3 mRNA expression in gastrocnemius muscle from diabetic rats was increased fourfold (P < 0.005), and the increase was prevented by insulin treatment. |
| 1495 | 10868941 | The effect of uncontrolled diabetes to decrease POMC, while increasing AgRP gene expression, suggests that reduced hypothalamic melanocortin signaling, along with increased NPY and decreased CRH signaling, could contribute to diabetic hyperphagia. |
| 1496 | 10892287 | Mutations in plasma membrane are involved in a large number of clinical disorders, including dwarfism, Laron syndrome, congenital hyperthyroidism or hypothyroidism, nephrogenic diabetes insipidus, resistance to TSH, LH, FSH and ACTH, Jansen's metaphyseal chondrodysplasia and autosomal dominant hypoparathyroidism. |
| 1497 | 10904142 | alpha-Melanocyte stimulating hormone prevents fasting-induced suppression of corticotropin-releasing hormone gene expression in the rat hypothalamic paraventricular nucleus. |
| 1498 | 10904142 | To test the hypothesis that the melanocortin system may be involved in the regulation of CRH mRNA in the PVN during fasting, the effect of intracerebroventricularly administered alpha-melanocyte stimulating hormone (MSH) on CRH mRNA in the PVN was studied in fasted animals by in situ hybridization histochemistry. |
| 1499 | 10904142 | Whereas fasting suppressed CRH mRNA levels in the PVN, alpha-MSH at doses of 150 and 300 ng every 6 h for 64 h prevented the fasting-induced suppression of CRH gene expression in the PVN. |
| 1500 | 10904142 | These data indicate that the suppression of alpha-MSH synthesis may be responsible for the decreased CRH gene expression in the PVN during fasting. |
| 1501 | 10904142 | alpha-Melanocyte stimulating hormone prevents fasting-induced suppression of corticotropin-releasing hormone gene expression in the rat hypothalamic paraventricular nucleus. |
| 1502 | 10904142 | To test the hypothesis that the melanocortin system may be involved in the regulation of CRH mRNA in the PVN during fasting, the effect of intracerebroventricularly administered alpha-melanocyte stimulating hormone (MSH) on CRH mRNA in the PVN was studied in fasted animals by in situ hybridization histochemistry. |
| 1503 | 10904142 | Whereas fasting suppressed CRH mRNA levels in the PVN, alpha-MSH at doses of 150 and 300 ng every 6 h for 64 h prevented the fasting-induced suppression of CRH gene expression in the PVN. |
| 1504 | 10904142 | These data indicate that the suppression of alpha-MSH synthesis may be responsible for the decreased CRH gene expression in the PVN during fasting. |
| 1505 | 10904142 | alpha-Melanocyte stimulating hormone prevents fasting-induced suppression of corticotropin-releasing hormone gene expression in the rat hypothalamic paraventricular nucleus. |
| 1506 | 10904142 | To test the hypothesis that the melanocortin system may be involved in the regulation of CRH mRNA in the PVN during fasting, the effect of intracerebroventricularly administered alpha-melanocyte stimulating hormone (MSH) on CRH mRNA in the PVN was studied in fasted animals by in situ hybridization histochemistry. |
| 1507 | 10904142 | Whereas fasting suppressed CRH mRNA levels in the PVN, alpha-MSH at doses of 150 and 300 ng every 6 h for 64 h prevented the fasting-induced suppression of CRH gene expression in the PVN. |
| 1508 | 10904142 | These data indicate that the suppression of alpha-MSH synthesis may be responsible for the decreased CRH gene expression in the PVN during fasting. |
| 1509 | 10904142 | alpha-Melanocyte stimulating hormone prevents fasting-induced suppression of corticotropin-releasing hormone gene expression in the rat hypothalamic paraventricular nucleus. |
| 1510 | 10904142 | To test the hypothesis that the melanocortin system may be involved in the regulation of CRH mRNA in the PVN during fasting, the effect of intracerebroventricularly administered alpha-melanocyte stimulating hormone (MSH) on CRH mRNA in the PVN was studied in fasted animals by in situ hybridization histochemistry. |
| 1511 | 10904142 | Whereas fasting suppressed CRH mRNA levels in the PVN, alpha-MSH at doses of 150 and 300 ng every 6 h for 64 h prevented the fasting-induced suppression of CRH gene expression in the PVN. |
| 1512 | 10904142 | These data indicate that the suppression of alpha-MSH synthesis may be responsible for the decreased CRH gene expression in the PVN during fasting. |
| 1513 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1514 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1515 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1516 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1517 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1518 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1519 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1520 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1521 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1522 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1523 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1524 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1525 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1526 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1527 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1528 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1529 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1530 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1531 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1532 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1533 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1534 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1535 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1536 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1537 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1538 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1539 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1540 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1541 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1542 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1543 | 10905492 | Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia. |
| 1544 | 10905492 | In situ hybridization for neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA was performed in sections of ARC containing maximal numbers of apoptotic cells as well as in other fresh frozen brains. |
| 1545 | 10905492 | After 1 bout, NPY (0.041+/-0.003) and POMC (0.119+/-0.022) mRNA were decreased, respectively, by 52 and 55% vs. controls (NPY 0.076+/-0.007; POMC 0.222+/-0.020; P = 0.01). |
| 1546 | 10905492 | NPY (0.029+/-0.002) but not POMC (0.093+/-0.013) fell 29% further after a third bout. |
| 1547 | 10905492 | NPY (r = -0.721; P = 0.001) and POMC (r = -0.756; P = 0.001) mRNA levels correlated negatively with the number of apoptotic ARC cells in the same sections. |
| 1548 | 10905492 | Thus, non-coma hypoglycemia produces apparent apoptotic cell death with reduced NPY and POMC expression selectively in the ARC. |
| 1549 | 10909960 | Leptin, expressed in adipose tissue, mediates some of its actions through several hypothalamic neuropeptides, notably agouti-related peptide, proopiomelanocortin, and neuropeptide Y. |
| 1550 | 10909960 | Expression of leptin is regulated by dietary status, insulin, and glucocorticoids. |
| 1551 | 10909960 | We report that MCH stimulates leptin mRNA expression and leptin secretion. |
| 1552 | 10909960 | MCH stimulated a 2-fold increase in leptin secretion by isolated rat adipocytes after 4 h of treatment. |
| 1553 | 10909960 | This increase in secreted leptin was preceded by a rapid and transient increase in ob mRNA levels; MCH stimulated a 2.5-fold increase in ob mRNA within 1 h of treatment, followed by a decline to basal levels within 4 h. |
| 1554 | 10909960 | In addition, we demonstrate that the MCH receptor SLC-1 is expressed in adipocytes, suggesting that fat cells may be targets of MCH or an MCH-like peptide under physiological conditions. |
| 1555 | 10926317 | Interleukin-6 is inhibited by glucocorticoids and stimulates ACTH secretion and POMC expression in human corticotroph pituitary adenomas. |
| 1556 | 10926317 | Here we examined the effects of IL-6 on propiomelanocortin (POMC) expression and ACTH production in corticotroph adenoma cells in vitro. |
| 1557 | 10926317 | We found that IL-6 stimulates both ACTH secretion and POMC gene expression in corticotroph adenoma cell cultures. |
| 1558 | 10926317 | This intratumoral produced IL-6 may be in part responsible, in an autocrine manner, for the stimulation of ACTH synthesis and secretion. |
| 1559 | 10926317 | However, elevated glucocorticoid levels in patients with Cushing's disease may prevent excessive action of IL-6 on ACTH production and tumor progression of corticotroph adenomas in vivo. |
| 1560 | 10926317 | Interleukin-6 is inhibited by glucocorticoids and stimulates ACTH secretion and POMC expression in human corticotroph pituitary adenomas. |
| 1561 | 10926317 | Here we examined the effects of IL-6 on propiomelanocortin (POMC) expression and ACTH production in corticotroph adenoma cells in vitro. |
| 1562 | 10926317 | We found that IL-6 stimulates both ACTH secretion and POMC gene expression in corticotroph adenoma cell cultures. |
| 1563 | 10926317 | This intratumoral produced IL-6 may be in part responsible, in an autocrine manner, for the stimulation of ACTH synthesis and secretion. |
| 1564 | 10926317 | However, elevated glucocorticoid levels in patients with Cushing's disease may prevent excessive action of IL-6 on ACTH production and tumor progression of corticotroph adenomas in vivo. |
| 1565 | 10926317 | Interleukin-6 is inhibited by glucocorticoids and stimulates ACTH secretion and POMC expression in human corticotroph pituitary adenomas. |
| 1566 | 10926317 | Here we examined the effects of IL-6 on propiomelanocortin (POMC) expression and ACTH production in corticotroph adenoma cells in vitro. |
| 1567 | 10926317 | We found that IL-6 stimulates both ACTH secretion and POMC gene expression in corticotroph adenoma cell cultures. |
| 1568 | 10926317 | This intratumoral produced IL-6 may be in part responsible, in an autocrine manner, for the stimulation of ACTH synthesis and secretion. |
| 1569 | 10926317 | However, elevated glucocorticoid levels in patients with Cushing's disease may prevent excessive action of IL-6 on ACTH production and tumor progression of corticotroph adenomas in vivo. |
| 1570 | 10926317 | Interleukin-6 is inhibited by glucocorticoids and stimulates ACTH secretion and POMC expression in human corticotroph pituitary adenomas. |
| 1571 | 10926317 | Here we examined the effects of IL-6 on propiomelanocortin (POMC) expression and ACTH production in corticotroph adenoma cells in vitro. |
| 1572 | 10926317 | We found that IL-6 stimulates both ACTH secretion and POMC gene expression in corticotroph adenoma cell cultures. |
| 1573 | 10926317 | This intratumoral produced IL-6 may be in part responsible, in an autocrine manner, for the stimulation of ACTH synthesis and secretion. |
| 1574 | 10926317 | However, elevated glucocorticoid levels in patients with Cushing's disease may prevent excessive action of IL-6 on ACTH production and tumor progression of corticotroph adenomas in vivo. |
| 1575 | 10926317 | Interleukin-6 is inhibited by glucocorticoids and stimulates ACTH secretion and POMC expression in human corticotroph pituitary adenomas. |
| 1576 | 10926317 | Here we examined the effects of IL-6 on propiomelanocortin (POMC) expression and ACTH production in corticotroph adenoma cells in vitro. |
| 1577 | 10926317 | We found that IL-6 stimulates both ACTH secretion and POMC gene expression in corticotroph adenoma cell cultures. |
| 1578 | 10926317 | This intratumoral produced IL-6 may be in part responsible, in an autocrine manner, for the stimulation of ACTH synthesis and secretion. |
| 1579 | 10926317 | However, elevated glucocorticoid levels in patients with Cushing's disease may prevent excessive action of IL-6 on ACTH production and tumor progression of corticotroph adenomas in vivo. |
| 1580 | 10989958 | The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man. |
| 1581 | 10989958 | After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period. |
| 1582 | 10989958 | ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074). |
| 1583 | 10989958 | Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin. |
| 1584 | 10989958 | The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man. |
| 1585 | 10989958 | The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man. |
| 1586 | 10989958 | After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period. |
| 1587 | 10989958 | ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074). |
| 1588 | 10989958 | Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin. |
| 1589 | 10989958 | The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man. |
| 1590 | 10989958 | The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man. |
| 1591 | 10989958 | After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period. |
| 1592 | 10989958 | ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074). |
| 1593 | 10989958 | Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin. |
| 1594 | 10989958 | The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man. |
| 1595 | 10989958 | The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man. |
| 1596 | 10989958 | After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period. |
| 1597 | 10989958 | ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074). |
| 1598 | 10989958 | Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin. |
| 1599 | 10989958 | The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man. |
| 1600 | 10989958 | The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man. |
| 1601 | 10989958 | After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period. |
| 1602 | 10989958 | ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074). |
| 1603 | 10989958 | Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin. |
| 1604 | 10989958 | The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man. |
| 1605 | 11024558 | We also determined whether well known hypothalamic neuropeptide targets, e.g. neuropeptide Y (NPY), proopiomelanocortin (POMC), agouti-related peptide (AGRP) and cocaine and amphetamine-regulated transcript (CART) were regulated in a pattern consistent with their presumed roles as mediators of leptin action. |
| 1606 | 11024558 | In contrast, leptin decreased body weight and adiposity, increased CART and suppressed NPY and AGRP mRNA expression in adult mice. |
| 1607 | 11078456 | Unlike leptin, ciliary neurotrophic factor does not reverse the starvation-induced changes of serum corticosterone and hypothalamic neuropeptide levels but induces expression of hypothalamic inhibitors of leptin signaling. |
| 1608 | 11078456 | Ciliary neurotrophic factor (CNTF), a cytokine closely related to leptin, reduces food intake and reverses obesity, but its role in restoring the starvation-induced changes of hormones or hypothalamic neuropeptides remains largely unknown. |
| 1609 | 11078456 | To comparatively assess the roles of CNTF and leptin in reversing the starvation-induced changes of hypothalamic neuropeptides and endocrine function and in inducing expression of hypothalamic inhibitors of leptin and CNTF signaling (suppressor of cytokine signaling 3 [SOCS-3]) and mediators of energy expenditure (cyclo-oxygenase 2 [COX-2]), we studied the effect of CNTF and leptin administered by intraperitoneal injections (1 microg/g twice daily) in C57Bl/6J mice fasted for 48 h. |
| 1610 | 11078456 | Serum corticosterone levels increased with fasting, and leptin administration partially normalized them, whereas CNTF administration had no effect. |
| 1611 | 11078456 | Hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) mRNA expression increased and pro-opiomelanocortin (POMC) decreased in response to fasting. |
| 1612 | 11078456 | Leptin administration decreased NPY and AgRP and increased POMC mRNA levels toward baseline, but CNTF administration in fasted mice had no effect of comparable significance. |
| 1613 | 11078456 | Both leptin and CNTF administration in fasted mice resulted in an induction of SOCS-3 mRNA expression. |
| 1614 | 11078456 | CNTF also induced hypothalamic SOCS-2 mRNA expression. |
| 1615 | 11078456 | Finally, neither leptin nor CNTF administration in mice fasted for 48 h alters hypothalamic COX-2 expression. |
| 1616 | 11078456 | Our data suggest that only falling leptin levels mediate the starvation-induced alterations in corticosterone levels and expression of hypothalamic neuropeptides, but inhibitors of leptin signaling are induced by both leptin and CNTF. |
| 1617 | 11078456 | Unlike leptin, ciliary neurotrophic factor does not reverse the starvation-induced changes of serum corticosterone and hypothalamic neuropeptide levels but induces expression of hypothalamic inhibitors of leptin signaling. |
| 1618 | 11078456 | Ciliary neurotrophic factor (CNTF), a cytokine closely related to leptin, reduces food intake and reverses obesity, but its role in restoring the starvation-induced changes of hormones or hypothalamic neuropeptides remains largely unknown. |
| 1619 | 11078456 | To comparatively assess the roles of CNTF and leptin in reversing the starvation-induced changes of hypothalamic neuropeptides and endocrine function and in inducing expression of hypothalamic inhibitors of leptin and CNTF signaling (suppressor of cytokine signaling 3 [SOCS-3]) and mediators of energy expenditure (cyclo-oxygenase 2 [COX-2]), we studied the effect of CNTF and leptin administered by intraperitoneal injections (1 microg/g twice daily) in C57Bl/6J mice fasted for 48 h. |
| 1620 | 11078456 | Serum corticosterone levels increased with fasting, and leptin administration partially normalized them, whereas CNTF administration had no effect. |
| 1621 | 11078456 | Hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) mRNA expression increased and pro-opiomelanocortin (POMC) decreased in response to fasting. |
| 1622 | 11078456 | Leptin administration decreased NPY and AgRP and increased POMC mRNA levels toward baseline, but CNTF administration in fasted mice had no effect of comparable significance. |
| 1623 | 11078456 | Both leptin and CNTF administration in fasted mice resulted in an induction of SOCS-3 mRNA expression. |
| 1624 | 11078456 | CNTF also induced hypothalamic SOCS-2 mRNA expression. |
| 1625 | 11078456 | Finally, neither leptin nor CNTF administration in mice fasted for 48 h alters hypothalamic COX-2 expression. |
| 1626 | 11078456 | Our data suggest that only falling leptin levels mediate the starvation-induced alterations in corticosterone levels and expression of hypothalamic neuropeptides, but inhibitors of leptin signaling are induced by both leptin and CNTF. |
| 1627 | 11078460 | Relative to lean controls, ob/ob mice also exhibit decreased hypothalamic proopiomelanocortin (POMC) mRNA and increased hypothalamic agouti-related peptide (AGRP) mRNA and neuropeptide Y (NPY) mRNA. |
| 1628 | 11078460 | In wild-type mice, adrenalectomy significantly decreased AGRP mRNA but did not significantly influence POMC or NPY mRNA. |
| 1629 | 11078460 | In ob/ob mice, adrenalectomy reduced the levels of plasma glucose, serum insulin and corticosterone, and food intake toward or below wild-type levels, and it restored hypothalamic POMC and AGRP mRNA but not NPY mRNA to wild-type levels. |
| 1630 | 11078460 | Relative to lean controls, ob/ob mice also exhibit decreased hypothalamic proopiomelanocortin (POMC) mRNA and increased hypothalamic agouti-related peptide (AGRP) mRNA and neuropeptide Y (NPY) mRNA. |
| 1631 | 11078460 | In wild-type mice, adrenalectomy significantly decreased AGRP mRNA but did not significantly influence POMC or NPY mRNA. |
| 1632 | 11078460 | In ob/ob mice, adrenalectomy reduced the levels of plasma glucose, serum insulin and corticosterone, and food intake toward or below wild-type levels, and it restored hypothalamic POMC and AGRP mRNA but not NPY mRNA to wild-type levels. |
| 1633 | 11078460 | Relative to lean controls, ob/ob mice also exhibit decreased hypothalamic proopiomelanocortin (POMC) mRNA and increased hypothalamic agouti-related peptide (AGRP) mRNA and neuropeptide Y (NPY) mRNA. |
| 1634 | 11078460 | In wild-type mice, adrenalectomy significantly decreased AGRP mRNA but did not significantly influence POMC or NPY mRNA. |
| 1635 | 11078460 | In ob/ob mice, adrenalectomy reduced the levels of plasma glucose, serum insulin and corticosterone, and food intake toward or below wild-type levels, and it restored hypothalamic POMC and AGRP mRNA but not NPY mRNA to wild-type levels. |
| 1636 | 11125000 | Association of cocaine- and amphetamine-regulated transcript-immunoreactive elements with thyrotropin-releasing hormone-synthesizing neurons in the hypothalamic paraventricular nucleus and its role in the regulation of the hypothalamic-pituitary-thyroid axis during fasting. |
| 1637 | 11125000 | Because cocaine- and amphetamine-regulated transcript (CART) coexists with alpha-melanocyte stimulating hormone (alpha-MSH) in the arcuate nucleus neurons and we have recently demonstrated that alpha-MSH innervates TRH-synthesizing neurons in the hypothalamic paraventricular nucleus (PVN), we raised the possibility that CART may also be contained in fibers that innervate hypophysiotropic thyrotropin-releasing hormone (TRH) neurons and modulate TRH gene expression. |
| 1638 | 11125000 | Triple-labeling fluorescent in situ hybridization and immunofluorescence were performed to reveal the morphological relationships between pro-TRH mRNA-containing neurons and CART- and alpha-MSH-immunoreactive (IR) axons. |
| 1639 | 11125000 | In addition, >80% of TRH/CART neurons in the periventricular and medial parvocellular subdivisions accumulated Fluoro-Gold after systemic administration, suggesting that CART may serve as a marker for hypophysiotropic TRH neurons. |
| 1640 | 11125000 | CART prevented fasting-induced suppression of pro-TRH in the PVN when administered intracerebroventricularly and increased the content of TRH in hypothalamic cell cultures. |
| 1641 | 11125000 | These studies establish an anatomical association between CART and pro-TRH-producing neurons in the PVN and demonstrate that CART has a stimulatory effect on hypophysiotropic TRH neurons by increasing pro-TRH gene expression and the biosynthesis of TRH. |
| 1642 | 11125000 | Association of cocaine- and amphetamine-regulated transcript-immunoreactive elements with thyrotropin-releasing hormone-synthesizing neurons in the hypothalamic paraventricular nucleus and its role in the regulation of the hypothalamic-pituitary-thyroid axis during fasting. |
| 1643 | 11125000 | Because cocaine- and amphetamine-regulated transcript (CART) coexists with alpha-melanocyte stimulating hormone (alpha-MSH) in the arcuate nucleus neurons and we have recently demonstrated that alpha-MSH innervates TRH-synthesizing neurons in the hypothalamic paraventricular nucleus (PVN), we raised the possibility that CART may also be contained in fibers that innervate hypophysiotropic thyrotropin-releasing hormone (TRH) neurons and modulate TRH gene expression. |
| 1644 | 11125000 | Triple-labeling fluorescent in situ hybridization and immunofluorescence were performed to reveal the morphological relationships between pro-TRH mRNA-containing neurons and CART- and alpha-MSH-immunoreactive (IR) axons. |
| 1645 | 11125000 | In addition, >80% of TRH/CART neurons in the periventricular and medial parvocellular subdivisions accumulated Fluoro-Gold after systemic administration, suggesting that CART may serve as a marker for hypophysiotropic TRH neurons. |
| 1646 | 11125000 | CART prevented fasting-induced suppression of pro-TRH in the PVN when administered intracerebroventricularly and increased the content of TRH in hypothalamic cell cultures. |
| 1647 | 11125000 | These studies establish an anatomical association between CART and pro-TRH-producing neurons in the PVN and demonstrate that CART has a stimulatory effect on hypophysiotropic TRH neurons by increasing pro-TRH gene expression and the biosynthesis of TRH. |
| 1648 | 11193441 | The plasma concentrations of GH, TSH, LH, FSH, ACTH and ADH were low or below the detectable limits. |
| 1649 | 11193441 | Arginine, LH-RH, TRH and CRH tolerance tests revealed no or low responses of GH, LH/FSH, TSH, and ACTH/cortisol, respectively. |
| 1650 | 11196419 | There is a progressive and concurrent increase of ACTH1-39 and cortisol (F) in the circulation of fetal sheep during the last 15-20 days of pregnancy (term, day 145-150) associated with increased expression of hypothalamic CRH pituitary POMC and adrenal ACTH receptor and steroidogenic enzymes, particularly P450 C17. |
| 1651 | 11272157 | To better understand the function(s) of the LEPR isoforms in vivo, we generated db3J/db3J and db/db mice bearing a transgene (neuron-specific enolase [NSE]-Rb) expressing the B isoform of LEPR, the isoform capable of activating the signal transducer and activator of transcription (STAT) pathway, under the control of the neuron-specific enolase enhancer/promoter. |
| 1652 | 11272157 | Based on quantitative analysis of hypothalamic neuropeptide gene expression in the transgenic animals, we infer full restoration of leptin sensitivity to proopiomelanocortin (POMC) neurons, partial correction of leptin sensitivity in agouti gene-related protein (AGRP)/neuropeptide Y (NPY) neurons, and a lack of effect on leptin sensitivity of melanin concentrating hormone neurons. |
| 1653 | 11272157 | Thus, hypothalamic POMC and AGRP/NPY neurons are primary candidates as the mediators of the effects of the NSE-Rb transgene on energy homeostasis, ingestive behavior, the neuroendocrine system, and glucose metabolism. |
| 1654 | 11272157 | To better understand the function(s) of the LEPR isoforms in vivo, we generated db3J/db3J and db/db mice bearing a transgene (neuron-specific enolase [NSE]-Rb) expressing the B isoform of LEPR, the isoform capable of activating the signal transducer and activator of transcription (STAT) pathway, under the control of the neuron-specific enolase enhancer/promoter. |
| 1655 | 11272157 | Based on quantitative analysis of hypothalamic neuropeptide gene expression in the transgenic animals, we infer full restoration of leptin sensitivity to proopiomelanocortin (POMC) neurons, partial correction of leptin sensitivity in agouti gene-related protein (AGRP)/neuropeptide Y (NPY) neurons, and a lack of effect on leptin sensitivity of melanin concentrating hormone neurons. |
| 1656 | 11272157 | Thus, hypothalamic POMC and AGRP/NPY neurons are primary candidates as the mediators of the effects of the NSE-Rb transgene on energy homeostasis, ingestive behavior, the neuroendocrine system, and glucose metabolism. |
| 1657 | 11281377 | IL-6 and its receptor IL-6R are co-expressed at similar sites in the human adrenal gland, which seems to be an important source of IL-6 production. |
| 1658 | 11281377 | This explains the high systemic cortisol levels in the absence of adequate plasma concentrations of corticotropin (ACTH) observed in patients after long-term treatment with IL-6. |
| 1659 | 11281377 | It could therefore be concluded that in situations of prolonged stress, when corticotropin-releasing hormone and ACTH release are suppressed by feedback inhibition due to circulating glucocorticoids, IL-6 maintains the elevated glucocorticoid levels by direct stimulation of adrenocortical steroidogenesis via autocrine/paracrine mechanisms. |
| 1660 | 11281377 | IL-6 and its receptor IL-6R are co-expressed at similar sites in the human adrenal gland, which seems to be an important source of IL-6 production. |
| 1661 | 11281377 | This explains the high systemic cortisol levels in the absence of adequate plasma concentrations of corticotropin (ACTH) observed in patients after long-term treatment with IL-6. |
| 1662 | 11281377 | It could therefore be concluded that in situations of prolonged stress, when corticotropin-releasing hormone and ACTH release are suppressed by feedback inhibition due to circulating glucocorticoids, IL-6 maintains the elevated glucocorticoid levels by direct stimulation of adrenocortical steroidogenesis via autocrine/paracrine mechanisms. |
| 1663 | 11289036 | However, in contrast to leptin, cerulenin did not prevent effects of fasting on plasma corticosterone or hypothalamic levels of neuropeptide Y, agouti-related peptide, pro-opiomelanocortin, or cocaine- and amphetamine-related peptide mRNA. |
| 1664 | 11314750 | Hormonal study revealed central diabetes insipidus, hypopituitarism, and slightly increased prolactin level. |
| 1665 | 11314750 | The pathological examinations revealed fibrous tissue with heavy inflammatory infiltrate composed of lymphocytes and plasma cells, islands of eosinophilic epithelial cells stained positively for chromogranin, GH, ACTH, and PRL and negatively for antibodies directed against HLA-II antigens. |
| 1666 | 11341305 | Age was positively correlated with IL-6 (female and male: p<0.001) and adrenocorticotropic hormone (ACTH) in women only (p<0.001). |
| 1667 | 11341305 | However, a linear regression analysis revealed that the increase of ACTH in relation to cortisol depends on serum free testosterone in men (p=0.042) and on serum free 17 beta-estradiol (p<0.001) together with serum IL-6 in women (p=0.021). |
| 1668 | 11341305 | The gender-specific changes of cortisol in relation to ACTH depend on the age-related decrease of the respective sex hormone in both gender groups and the increase of IL-6 in women. |
| 1669 | 11341305 | Age was positively correlated with IL-6 (female and male: p<0.001) and adrenocorticotropic hormone (ACTH) in women only (p<0.001). |
| 1670 | 11341305 | However, a linear regression analysis revealed that the increase of ACTH in relation to cortisol depends on serum free testosterone in men (p=0.042) and on serum free 17 beta-estradiol (p<0.001) together with serum IL-6 in women (p=0.021). |
| 1671 | 11341305 | The gender-specific changes of cortisol in relation to ACTH depend on the age-related decrease of the respective sex hormone in both gender groups and the increase of IL-6 in women. |
| 1672 | 11341305 | Age was positively correlated with IL-6 (female and male: p<0.001) and adrenocorticotropic hormone (ACTH) in women only (p<0.001). |
| 1673 | 11341305 | However, a linear regression analysis revealed that the increase of ACTH in relation to cortisol depends on serum free testosterone in men (p=0.042) and on serum free 17 beta-estradiol (p<0.001) together with serum IL-6 in women (p=0.021). |
| 1674 | 11341305 | The gender-specific changes of cortisol in relation to ACTH depend on the age-related decrease of the respective sex hormone in both gender groups and the increase of IL-6 in women. |
| 1675 | 11572327 | Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II. |
| 1676 | 11572327 | With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests. |
| 1677 | 11572327 | Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion. |
| 1678 | 11572327 | An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable. |
| 1679 | 11572327 | Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II. |
| 1680 | 11572327 | With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests. |
| 1681 | 11572327 | Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion. |
| 1682 | 11572327 | An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable. |
| 1683 | 11572327 | Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II. |
| 1684 | 11572327 | With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests. |
| 1685 | 11572327 | Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion. |
| 1686 | 11572327 | An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable. |
| 1687 | 11581309 | Conscious rats received week-long infusions of either a melanocortin receptor agonist, alpha-melanocyte-stimulating hormone (alpha-MSH), or antagonist, SHU9119, in the third cerebral ventricle while food intake was maintained constant in each group. alpha-MSH decreased intra-abdominal fat and markedly enhanced the actions of insulin on both glucose uptake and production, while SHU9119 exerted opposite effects. |
| 1688 | 11606455 | Increased ACTH with diabetes corresponded with increased hypothalamic CRH mRNA, but no change in pituitary POMC mRNA. |
| 1689 | 11606455 | With insulin-treatment, CRH mRNA remained elevated, and POMC mRNA was unaltered. |
| 1690 | 11606455 | We postulate that, in STZ-diabetes: 1) increased HPA activity is caused by increased central drive at and/or above the level of the paraventricular nucleus and is associated with decreased epinephrine; and 2) normalized pituitary-adrenal activity with insulin may be caused by the compensatory increase in GR mRNA allowing glucocorticoid-mediated suppression of ACTH secretion despite the residual increase in central HPA activity. |
| 1691 | 11606455 | Increased ACTH with diabetes corresponded with increased hypothalamic CRH mRNA, but no change in pituitary POMC mRNA. |
| 1692 | 11606455 | With insulin-treatment, CRH mRNA remained elevated, and POMC mRNA was unaltered. |
| 1693 | 11606455 | We postulate that, in STZ-diabetes: 1) increased HPA activity is caused by increased central drive at and/or above the level of the paraventricular nucleus and is associated with decreased epinephrine; and 2) normalized pituitary-adrenal activity with insulin may be caused by the compensatory increase in GR mRNA allowing glucocorticoid-mediated suppression of ACTH secretion despite the residual increase in central HPA activity. |
| 1694 | 11606455 | Increased ACTH with diabetes corresponded with increased hypothalamic CRH mRNA, but no change in pituitary POMC mRNA. |
| 1695 | 11606455 | With insulin-treatment, CRH mRNA remained elevated, and POMC mRNA was unaltered. |
| 1696 | 11606455 | We postulate that, in STZ-diabetes: 1) increased HPA activity is caused by increased central drive at and/or above the level of the paraventricular nucleus and is associated with decreased epinephrine; and 2) normalized pituitary-adrenal activity with insulin may be caused by the compensatory increase in GR mRNA allowing glucocorticoid-mediated suppression of ACTH secretion despite the residual increase in central HPA activity. |
| 1697 | 11686544 | Our series exemplifies the wide spectrum of LCH-induced hypopituitarism, and demonstrates some unique features, including a higher incidence of CRH/ACTH deficiency compared to other reports (4/7 patients), and massive obesity in 2 of our patients. |
| 1698 | 11730986 | Up-regulation of splenic prohormone convertases PC1 and PC2 in diabetic rats. |
| 1699 | 11730986 | To test this hypothesis, we treated rats with intraperitoneal streptozotocin (STZ) (50 mg/kg/day) daily for 5 days and measured splenic PC1 and PC2 mRNA by ribonuclease protection assay. |
| 1700 | 11730986 | We found that PC1 mRNA was increased 6.0+/-0.02-fold (P<0.05) and PC2 mRNA was increased 1.80+/-0.01-fold (P<0.005) in the spleen of rats that received STZ compared to rats that received vehicle. |
| 1701 | 11730986 | PC2 and pro-opiomelanocortin (POMC, a possible splenic substrate for PC1/PC2) immunoreactivity was found predominantly in the red pulp. |
| 1702 | 11730986 | STZ induced an increase in splenic PC1 and POMC, but not PC2 protein levels. |
| 1703 | 11730986 | Up-regulation of splenic prohormone convertases PC1 and PC2 in diabetic rats. |
| 1704 | 11730986 | To test this hypothesis, we treated rats with intraperitoneal streptozotocin (STZ) (50 mg/kg/day) daily for 5 days and measured splenic PC1 and PC2 mRNA by ribonuclease protection assay. |
| 1705 | 11730986 | We found that PC1 mRNA was increased 6.0+/-0.02-fold (P<0.05) and PC2 mRNA was increased 1.80+/-0.01-fold (P<0.005) in the spleen of rats that received STZ compared to rats that received vehicle. |
| 1706 | 11730986 | PC2 and pro-opiomelanocortin (POMC, a possible splenic substrate for PC1/PC2) immunoreactivity was found predominantly in the red pulp. |
| 1707 | 11730986 | STZ induced an increase in splenic PC1 and POMC, but not PC2 protein levels. |
| 1708 | 11735084 | Specific binding sites for [125I]beta-endorphin and the delta1-opioid [3H][D-pen(2), D-pen(5)]enkephalin (DPDPE) were quantified using autoradiography in soleus and extensor digitorum longus (EDL) muscles of lean and obese-diabetic (ob/ob) mice. |
| 1709 | 11739434 | To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). |
| 1710 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1711 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1712 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1713 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1714 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1715 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1716 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1717 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1718 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1719 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1720 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1721 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1722 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1723 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1724 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1725 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1726 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1727 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1728 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1729 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1730 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1731 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1732 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1733 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1734 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1735 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1736 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1737 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1738 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1739 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1740 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1741 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1742 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1743 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1744 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1745 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1746 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1747 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1748 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1749 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1750 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1751 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1752 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1753 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1754 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1755 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1756 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1757 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1758 | 11748490 | The intrapituitary stimulatory effect of lipopolysaccharide on ACTH secretion is mediated by paracrine-acting IL-6. |
| 1759 | 11748490 | We have shown recently that LPS stimulates intrapituitary IL-6 production in folliculostellate cells via specific receptors and the p38a mitogen-activated protein kinase/nuclear factor-kappa B pathway. |
| 1760 | 11748490 | To test the physiological relevance of these findings, we studied whether LPS could enhance ACTH secretion via paracrine-acting intrapituitary IL-6. |
| 1761 | 11748490 | Lipopolysaccharide stimulated IL-6 secretion both in monolayer and aggregate mouse pituitary cell cultures, but only in aggregates, ACTH secretion was significantly enhanced by LPS. |
| 1762 | 11748490 | My4, an antibody that blocks the interaction of LPS with the LPS receptor CD14, suppressed both LPS-induced IL-6 and ACTH secretion in aggregate cultures. |
| 1763 | 11748490 | A neutralizing antibody against mouse IL-6 also inhibited LPS-induced ACTH secretion in aggregates. |
| 1764 | 11748490 | In mouse pituitary fragments, LPS-induced ACTH secretion was blocked by My4 and IL-6 antibodies, identically to re-aggregate cell cultures. |
| 1765 | 11748490 | LPS-induced ACTH secretion, mediated by intrapituitary IL-6, may represent a pituitary-specific mechanism that stimulates the HPA axis during infection/inflammation. |
| 1766 | 11770265 | Laboratory values were compatible with anterior (abnormal concentrations of adrenocorticotropin hormone, thyroid stimulating hormone, prolactin) and posterior (diabetes insipidus) pituitary gland insufficiency. |
| 1767 | 11790431 | This review will discuss this functional diversity by illustrating hypothalamic neurones that express neuropeptide Y (NPY), the melanocortin-4 receptor (MC4-R) and the orexins. |
| 1768 | 11790431 | NPY neurones in the arcuate nucleus (ARC) release NPY, a powerful inducer of feeding and obesity, in the paraventricular nucleus (PVN) and the lateral hypothalamic area (LHA). |
| 1769 | 11790431 | ARC-NPY neurones are inhibited by leptin and insulin and become overactive when levels of these hormones fall during undernutrition. |
| 1770 | 11790431 | With disruption of the inhibitory leptin signals due to gene mutations, the NPY neurones are overactive, which contributes to hyperphagia and obesity in the ob/ob and db/db mice and fa/fa Zucker rat. |
| 1771 | 11790431 | The MC4-R is activated by alpha-melanocyte-stimulating hormone [alpha-MSH; a cleavage product of pro-opiomelanocortin (POMC), which is expressed in the other ARC neurones] and inhibits feeding. |
| 1772 | 11790431 | Activation of MC4-R, possibly mediated by blockade of AGRP release, appears to restrain overeating of a palatable diet. |
| 1773 | 11790431 | Orexin-A and -B (corresponding to hypocretins 1 and 2) are expressed in specific LHA neurones. |
| 1774 | 11790431 | Orexin neurones also have close anatomical connections with LHA glucose-sensitive neurones. |
| 1775 | 11796185 | The content of beta-endorphin-like immunoreactivity (BER) in the adrenal medulla, determined by enzyme-linked immunosorbent assay, was actually higher in diabetic rats with insulin deficiency. |
| 1776 | 11796185 | Normalization of the plasma glucose concentration in STZ-diabetic rats with exogenous insulin or phlorizin, an inhibitor of the renal tubular glucose transport, reversed the mRNA level of POMC in the adrenal gland after 4 days of treatment. |
| 1777 | 11796185 | The content of beta-endorphin-like immunoreactivity (BER) in the adrenal medulla, determined by enzyme-linked immunosorbent assay, was actually higher in diabetic rats with insulin deficiency. |
| 1778 | 11796185 | Normalization of the plasma glucose concentration in STZ-diabetic rats with exogenous insulin or phlorizin, an inhibitor of the renal tubular glucose transport, reversed the mRNA level of POMC in the adrenal gland after 4 days of treatment. |
| 1779 | 11837451 | Its effect on pigmentation is achieved by antagonizing the binding of alpha-melanocyte stimulating hormone (alpha-MSH) to melanocortin 1 receptor (Mc1r), switching melanin synthesis from eumelanin (black/brown) to phaeomelanin (red/yellow). |
| 1780 | 11837451 | The yellow coat colour is the result of agouti chronically antagonizing the binding of alpha-MSH to Mc1r and the obese phenotype results from agouti protein antagonizing the binding of alpha-MSH to Mc3r and/or Mc4r. |
| 1781 | 11837451 | Its effect on pigmentation is achieved by antagonizing the binding of alpha-melanocyte stimulating hormone (alpha-MSH) to melanocortin 1 receptor (Mc1r), switching melanin synthesis from eumelanin (black/brown) to phaeomelanin (red/yellow). |
| 1782 | 11837451 | The yellow coat colour is the result of agouti chronically antagonizing the binding of alpha-MSH to Mc1r and the obese phenotype results from agouti protein antagonizing the binding of alpha-MSH to Mc3r and/or Mc4r. |
| 1783 | 11857909 | Mutations in GPCRs have been associated with dwarfism, congenital hyperthyroidism or hypothyroidism, nephrogenic diabetes insipidus, obesity, resistance to TSH, LH, FSH and ACTH, Jansen's metaphyseal and Blomstrand's chondrodysplasia, autosomal dominant hypoparathyroidism, and neonatal severe hyperparathyroidism. |
| 1784 | 11857909 | Mutations in other families of receptors which are characterized into one spanning-transmembrane receptor can result in resistance to insulin, GH, leptin and AMH. |
| 1785 | 11857934 | [Obesity induced by abnormality in leptin receptor and melanocortin-4 receptor]. |
| 1786 | 11857934 | Leptin directly exerts its anorexigenic effects on hypothalamic arcuate nucleus. alpha-melanocyte stimulating hormone (alpha-MSH) derived from proopiomelanocortin (POMC) and melanocortin-4 receptor (MC4-R) have been reported to be involved in the downstream of leptin actions. |
| 1787 | 11857934 | In this paper, we summarize the clinical characteristics and the mechanisms of obesity caused by genetic abnormalities in leptin receptor and melanocortin-4 receptor. |
| 1788 | 11872679 | To investigate whether differences in hypothalamic melanocortin signaling can explain this discrepancy, we used in situ hybridization to compare the effects of STZ-diabetes and fasting on pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) mRNA levels in the hypothalamic arcuate nucleus (ARC) of Npy(--/--) and Npy(+/+) mice. |
| 1789 | 11872679 | STZ-diabetes also lowered POMC mRNA levels by 65% in the ARC of Npy(+/+) mice (P less-than-or-equal 0.05) but by only 11% in Npy(--/--) mice (NS); fasting significantly lowered POMC mRNA levels in both genotypes. |
| 1790 | 11872679 | We conclude that NPY is required for both the increase of food intake and the decrease of hypothalamic POMC gene expression induced by uncontrolled diabetes. |
| 1791 | 11872679 | To investigate whether differences in hypothalamic melanocortin signaling can explain this discrepancy, we used in situ hybridization to compare the effects of STZ-diabetes and fasting on pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) mRNA levels in the hypothalamic arcuate nucleus (ARC) of Npy(--/--) and Npy(+/+) mice. |
| 1792 | 11872679 | STZ-diabetes also lowered POMC mRNA levels by 65% in the ARC of Npy(+/+) mice (P less-than-or-equal 0.05) but by only 11% in Npy(--/--) mice (NS); fasting significantly lowered POMC mRNA levels in both genotypes. |
| 1793 | 11872679 | We conclude that NPY is required for both the increase of food intake and the decrease of hypothalamic POMC gene expression induced by uncontrolled diabetes. |
| 1794 | 11872679 | To investigate whether differences in hypothalamic melanocortin signaling can explain this discrepancy, we used in situ hybridization to compare the effects of STZ-diabetes and fasting on pro-opiomelanocortin (POMC) and agouti-related peptide (AgRP) mRNA levels in the hypothalamic arcuate nucleus (ARC) of Npy(--/--) and Npy(+/+) mice. |
| 1795 | 11872679 | STZ-diabetes also lowered POMC mRNA levels by 65% in the ARC of Npy(+/+) mice (P less-than-or-equal 0.05) but by only 11% in Npy(--/--) mice (NS); fasting significantly lowered POMC mRNA levels in both genotypes. |
| 1796 | 11872679 | We conclude that NPY is required for both the increase of food intake and the decrease of hypothalamic POMC gene expression induced by uncontrolled diabetes. |
| 1797 | 11924926 | In humans, mutations in leptin, leptin receptor, proopiomelanocortin (POMC), melanocortin-4 receptor (MC4R) and prohormone convertase 1 (PC1) have been described in patients with severe obesity. |
| 1798 | 11924926 | Most of these obesity disorders, with the exception of the MC4R mutations, exhibit recessive inheritance and a distinct phenotype with varying degrees of hypothalamic dysfunction, and they unravel the critical role of the central leptin and melanocortin pathways in human appetite control and energy homeostasis. |
| 1799 | 11924926 | To date, six MODY genes have been identified, the glucokinase gene and five beta cell-specific transcription factor genes, hepatocyte nuclear factor-1alpha (HNF-1alpha), HNF-1beta, HNF-4alpha, insulin promoter factor-1 (IPF-1) and NeuroD1/BETA2. |
| 1800 | 11924926 | At the other end of the spectrum are the inherited syndromes of insulin resistance that are caused by mutations in the insulin receptor gene and in the adipocyte-specific transcription factor PPARgamma. |
| 1801 | 11932281 | Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. |
| 1802 | 11932281 | In the present study we tested the hypothesis that metformin therapy in obese adolescents with PCOS will attenuate the adrenal steroidogenic response to ACTH, with reduction of insulin resistance/insulinemia. |
| 1803 | 11932281 | Pre- and posttherapy they had oral glucose tolerance testing, ACTH stimulation test, a 3-h hyperinsulinemic (80 mU/m(2).min)-euglycemic clamp to assess insulin sensitivity and a hyperglycemic clamp to assess insulin secretion. |
| 1804 | 11932281 | Fasting insulin correlated with the 17-hydroxypregnenelone response to ACTH stimulation (r = 0.52; P = 0.008). |
| 1805 | 11932281 | Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. |
| 1806 | 11932281 | In the present study we tested the hypothesis that metformin therapy in obese adolescents with PCOS will attenuate the adrenal steroidogenic response to ACTH, with reduction of insulin resistance/insulinemia. |
| 1807 | 11932281 | Pre- and posttherapy they had oral glucose tolerance testing, ACTH stimulation test, a 3-h hyperinsulinemic (80 mU/m(2).min)-euglycemic clamp to assess insulin sensitivity and a hyperglycemic clamp to assess insulin secretion. |
| 1808 | 11932281 | Fasting insulin correlated with the 17-hydroxypregnenelone response to ACTH stimulation (r = 0.52; P = 0.008). |
| 1809 | 11932281 | Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. |
| 1810 | 11932281 | In the present study we tested the hypothesis that metformin therapy in obese adolescents with PCOS will attenuate the adrenal steroidogenic response to ACTH, with reduction of insulin resistance/insulinemia. |
| 1811 | 11932281 | Pre- and posttherapy they had oral glucose tolerance testing, ACTH stimulation test, a 3-h hyperinsulinemic (80 mU/m(2).min)-euglycemic clamp to assess insulin sensitivity and a hyperglycemic clamp to assess insulin secretion. |
| 1812 | 11932281 | Fasting insulin correlated with the 17-hydroxypregnenelone response to ACTH stimulation (r = 0.52; P = 0.008). |
| 1813 | 11932281 | Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. |
| 1814 | 11932281 | In the present study we tested the hypothesis that metformin therapy in obese adolescents with PCOS will attenuate the adrenal steroidogenic response to ACTH, with reduction of insulin resistance/insulinemia. |
| 1815 | 11932281 | Pre- and posttherapy they had oral glucose tolerance testing, ACTH stimulation test, a 3-h hyperinsulinemic (80 mU/m(2).min)-euglycemic clamp to assess insulin sensitivity and a hyperglycemic clamp to assess insulin secretion. |
| 1816 | 11932281 | Fasting insulin correlated with the 17-hydroxypregnenelone response to ACTH stimulation (r = 0.52; P = 0.008). |
| 1817 | 11956158 | Administration of CRH and ACTH revealed reduced pituitary and adrenal sensitivity in untreated diabetic animals compared with both control and insulin-treated diabetic animals. |
| 1818 | 11959420 | In the paraventricular nucleus, CART mRNA is colocalized with vasopressin and corticotropin-releasing factor-containing neurons. |
| 1819 | 12031953 | We recently established that in addition to plasma adrenocorticotrophic hormone (ACTH) and corticosterone, hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal type 1 glucocorticoid receptor (GR1) mRNA were also upregulated in uncontrolled streptozotocin-induced diabetes. |
| 1820 | 12031953 | Insulin treatment restored ACTH and corticosterone but not epinephrine responses to hypoglycemia in diabetic rats. |
| 1821 | 12031953 | In response to hypoglycemia, hypothalamic CRH mRNA and pituitary proopiomelanocortin mRNA expression increased in control and insulin-treated but not in untreated diabetic rats. |
| 1822 | 12031953 | We recently established that in addition to plasma adrenocorticotrophic hormone (ACTH) and corticosterone, hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal type 1 glucocorticoid receptor (GR1) mRNA were also upregulated in uncontrolled streptozotocin-induced diabetes. |
| 1823 | 12031953 | Insulin treatment restored ACTH and corticosterone but not epinephrine responses to hypoglycemia in diabetic rats. |
| 1824 | 12031953 | In response to hypoglycemia, hypothalamic CRH mRNA and pituitary proopiomelanocortin mRNA expression increased in control and insulin-treated but not in untreated diabetic rats. |
| 1825 | 12031953 | We recently established that in addition to plasma adrenocorticotrophic hormone (ACTH) and corticosterone, hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal type 1 glucocorticoid receptor (GR1) mRNA were also upregulated in uncontrolled streptozotocin-induced diabetes. |
| 1826 | 12031953 | Insulin treatment restored ACTH and corticosterone but not epinephrine responses to hypoglycemia in diabetic rats. |
| 1827 | 12031953 | In response to hypoglycemia, hypothalamic CRH mRNA and pituitary proopiomelanocortin mRNA expression increased in control and insulin-treated but not in untreated diabetic rats. |
| 1828 | 12086933 | Double-label in situ hybridization demonstrated neuron-specific GK mRNA expression in locus ceruleus norepinephrine and in hypothalamic neuropeptide Y, pro-opiomelanocortin, and gamma-aminobutyric acid neurons, but it did not demonstrate this expression in orexin neurons. |
| 1829 | 12107209 | Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. |
| 1830 | 12107209 | The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. |
| 1831 | 12107209 | The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. |
| 1832 | 12107209 | The mean nonstimulated ACTH and cortisol concentrations were, respectively, 6.0 +/- 3.4 pmol/liter and 680 +/- 280 nmol/liter before leptin and did not change after 4 months of therapy (4.2 +/- 1.2 pmol/liter, P = 0.11 and 453 +/- 142 nmol/liter, P = 0.13, respectively). |
| 1833 | 12107209 | The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. |
| 1834 | 12107209 | Leptin replacement improved menstrual abnormalities and low E2 levels and corrected the attenuated LH response to LHRH in a group of young women with lipodystrophy and leptin deficiency. |
| 1835 | 12107209 | Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. |
| 1836 | 12107209 | The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. |
| 1837 | 12107209 | The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. |
| 1838 | 12107209 | The mean nonstimulated ACTH and cortisol concentrations were, respectively, 6.0 +/- 3.4 pmol/liter and 680 +/- 280 nmol/liter before leptin and did not change after 4 months of therapy (4.2 +/- 1.2 pmol/liter, P = 0.11 and 453 +/- 142 nmol/liter, P = 0.13, respectively). |
| 1839 | 12107209 | The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. |
| 1840 | 12107209 | Leptin replacement improved menstrual abnormalities and low E2 levels and corrected the attenuated LH response to LHRH in a group of young women with lipodystrophy and leptin deficiency. |
| 1841 | 12111488 | Endocrinological outcome following first time transsphenoidal surgery for GH-, ACTH-, and PRL-secreting pituitary adenomas. |
| 1842 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1843 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1844 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1845 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1846 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1847 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1848 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1849 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1850 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1851 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1852 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1853 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1854 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1855 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1856 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1857 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1858 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1859 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1860 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1861 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1862 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1863 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1864 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1865 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1866 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1867 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1868 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1869 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1870 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1871 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1872 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1873 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1874 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1875 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1876 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1877 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1878 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1879 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1880 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1881 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1882 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1883 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1884 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1885 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1886 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1887 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1888 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1889 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1890 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1891 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1892 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1893 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1894 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1895 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1896 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1897 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1898 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1899 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1900 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1901 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1902 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1903 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1904 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1905 | 12113951 | Intracerebroventricular administration of alpha-melanocyte stimulating hormone increases phosphorylation of CREB in TRH- and CRH-producing neurons of the hypothalamic paraventricular nucleus. |
| 1906 | 12113951 | Among these effects, fasting reduces TRH gene expression selectively in the hypothalamic paraventricular nucleus (PVN), which can be reversed by leptin administration. |
| 1907 | 12113951 | Intracerebroventricular (i.c.v.) infusion of alpha-MSH recapitulates the effects of leptin on hypophysiotropic TRH neurons, completely restoring proTRH mRNA to levels in fed animals despite continuation of the fast, making alpha-MSH a candidate for mediating the central effects of leptin. |
| 1908 | 12113951 | As alpha-MSH binds to a G-protein coupled receptor that activates cAMP and alpha-MSH stimulates the TRH promoter through the phosphorylation of the transcription factor CREB in vitro, we determined whether i.c.v. injection of alpha-MSH to rats regulates phosphorylation of CREB, specifically in hypophysiotropic TRH neurons of PVN. |
| 1909 | 12113951 | As alpha-MSH also induces the activation of CRH gene expression in the PVN, we further determined whether i.c.v. injection of alpha-MSH regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1910 | 12113951 | Double immunolabeling with proTRH antiserum revealed that following i.c.v. alpha-MSH infusion at 10 min, the majority of TRH neurons contained PCREB in the anterior (71%), medial (83%) and periventricular (63%) parvocellular subdivisions. |
| 1911 | 12113951 | The percentage of double-labeled TRH neurons declined at 30 min and 1 h post alpha-MSH infusion. |
| 1912 | 12113951 | Similarly, only 16% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle treated animals, whereas 10 min following alpha-MSH infusion the percentage of CRH neurons colocalizing with the PCREB rose to 54%, then fell to 37 and 17% at 30 and 60 min postinfusion, respectively. |
| 1913 | 12113951 | These data demonstrate that i.c.v. alpha-MSH administration increases the phosphorylation of CREB in several subdivisions of the PVN including TRH and CRH neurons in the medial and periventricular parvocellular subdivisions, suggesting that phosphorylation of CREB may be necessary for alpha-MSH-induced activation of the TRH and CRH genes. |
| 1914 | 12147141 | Meal size is controlled by a series of short-term hormonal and neural signals that derive from the gastrointestinal tract, such as cholecystokinin whereas others may initiate meals, such as the recently discovered hormone, ghrelin. |
| 1915 | 12147141 | Other hormones such as insulin and leptin, together with circulating nutrients, indicate long-term energy stores. |
| 1916 | 12147141 | When energy stores are low, production of leptin from adipose tissue, and thus circulating leptin concentrations fall, leading to increased production of hypothalamic neurotransmitters that strongly increase food intake, such as neuropeptide Y (NPY), galanin and agouti-related protein (AGRP) and decreased levels of alpha-melanocyte-stimulating hormone (alpha-MSH), cocaine and amphetamine-regulated transcript (CART) and neurotensin that reduce food intake and increase energy expenditure. |
| 1917 | 12147141 | The finding that mutations in leptin and POMC lead to severe early onset obesity in humans has highlighted the importance of these peptides in humans. |
| 1918 | 12147141 | Meal size is controlled by a series of short-term hormonal and neural signals that derive from the gastrointestinal tract, such as cholecystokinin whereas others may initiate meals, such as the recently discovered hormone, ghrelin. |
| 1919 | 12147141 | Other hormones such as insulin and leptin, together with circulating nutrients, indicate long-term energy stores. |
| 1920 | 12147141 | When energy stores are low, production of leptin from adipose tissue, and thus circulating leptin concentrations fall, leading to increased production of hypothalamic neurotransmitters that strongly increase food intake, such as neuropeptide Y (NPY), galanin and agouti-related protein (AGRP) and decreased levels of alpha-melanocyte-stimulating hormone (alpha-MSH), cocaine and amphetamine-regulated transcript (CART) and neurotensin that reduce food intake and increase energy expenditure. |
| 1921 | 12147141 | The finding that mutations in leptin and POMC lead to severe early onset obesity in humans has highlighted the importance of these peptides in humans. |
| 1922 | 12208672 | Further analysis in ACTH-stimulated bovine adrenal cells using stable isotope dilution/gas chromatography-mass spectrometry demonstrated CLO-induced inhibition of adrenal 21-hydroxylase (P450c21) activity leading to a dose-dependent increase in the 17-OH-progesterone/11-deoxycortisol ratio. |
| 1923 | 12351426 | Ghrelin is not necessary for adequate hormonal counterregulation of insulin-induced hypoglycemia. |
| 1924 | 12351426 | Ghrelin is a novel enteric hormone that stimulates growth hormone (GH), ACTH, and epinephrine; augments plasma glucose; and increases food intake by inducing the feeling of hunger. |
| 1925 | 12351426 | At present, it is not known whether ghrelin increases in response to insulin-induced hypoglycemia. |
| 1926 | 12351426 | To answer this question, we compared plasma ghrelin concentrations after a short-term insulin infusion that was allowed or not (euglycemic clamp) to cause hypoglycemia (2.7 +/- 0.2 mmol/l at 30 min) in five healthy volunteers. |
| 1927 | 12351426 | In both studies, plasma ghrelin concentrations decreased (P < 0.01) after insulin infusion (hypoglycemia by 14%, euglycemia by 22%), reached a nadir at 30 min, and returned to baseline at 60 min, without differences between the hypoglycemia and the euglycemia studies. |
| 1928 | 12351426 | There was a strong correlation (R(2) = 0.91, P < 0.002) between the insulin sensitivity of the subjects and the percentage suppression of ghrelin from baseline. |
| 1929 | 12351426 | These data demonstrate that ghrelin is not required for the hormonal defenses against insulin-induced hypoglycemia and that insulin can suppress ghrelin levels in healthy humans. |
| 1930 | 12359499 | The key findings included 1) that the coat color phenotype in the lethal yellow (A(Y)/a) mouse is due to antagonism of the melanocortin-1 receptor (MC1R) by the agouti gene product; 2) the MC3R and MC4R are expressed in CNS centers involved in energy homeostasis, and 3) the combined results of pharmacological studies showing that agouti is an antagonist of the MC4R and transgenic studies showing that inhibition or loss of the MC4R recapitulate the lethal yellow phenotype. |
| 1931 | 12359499 | Pro-opiomelanocortin (POMC), MC3R, and MC4R knockouts are obese and are now being used to further analyze melanocortin receptor function. |
| 1932 | 12359499 | The obesity phenotype observed in the MC3R and MC4R knockouts (KO) differ markedly. |
| 1933 | 12377295 | The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. |
| 1934 | 12377295 | CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. |
| 1935 | 12377295 | They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. |
| 1936 | 12377295 | The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. |
| 1937 | 12377295 | CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. |
| 1938 | 12377295 | They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. |
| 1939 | 12397532 | The Involvement of GABAA receptors in the control of GnRH and beta-endorphin release, and catecholaminergic activity in the preoptic area in anestrous ewes. |
| 1940 | 12397532 | This study examined role of GABA A receptors in the control of GnRH, beta-endorphin release and catecholaminergic system activity in the preoptic area and LH secretion in anestrous ewes. |
| 1941 | 12397532 | The decrease of LH pulse frequency and concentration of this hormone in blood plasma suggests that GABA A receptor agonist applied in the MPOA suppresses GnRH release from the GnRH axon terminals in the ventromedial hypothalamus-nucleus infundibularis region (VEN/NI) into the hypophyseal vascular system. |
| 1942 | 12397532 | These results suggest that suppression of GnRH/LH release during muscimol treatment may result from activation of GABA A receptors on the GnRH perikarya and/or through GABA A receptor mechanism on the dopaminergic and noradrenergic system in the MPOA. |
| 1943 | 12397532 | The Involvement of GABAA receptors in the control of GnRH and beta-endorphin release, and catecholaminergic activity in the preoptic area in anestrous ewes. |
| 1944 | 12397532 | This study examined role of GABA A receptors in the control of GnRH, beta-endorphin release and catecholaminergic system activity in the preoptic area and LH secretion in anestrous ewes. |
| 1945 | 12397532 | The decrease of LH pulse frequency and concentration of this hormone in blood plasma suggests that GABA A receptor agonist applied in the MPOA suppresses GnRH release from the GnRH axon terminals in the ventromedial hypothalamus-nucleus infundibularis region (VEN/NI) into the hypophyseal vascular system. |
| 1946 | 12397532 | These results suggest that suppression of GnRH/LH release during muscimol treatment may result from activation of GABA A receptors on the GnRH perikarya and/or through GABA A receptor mechanism on the dopaminergic and noradrenergic system in the MPOA. |
| 1947 | 12403080 | Leptin and insulin action in the central nervous system. |
| 1948 | 12403080 | This review summarizes old and recent data implicating insulin and leptin as key circulating signals to the central nervous system, particularly the ventral hypothalamus, in communicating the size and the distribution of body fat stores. |
| 1949 | 12403080 | The key primary neurons in the arcuate nucleus containing NPY/AgRP and POMC/CART appear be critical constituents of the CNS regulating system, and are shown to contribute to anabolic and catabolic signaling systems to complete the feedback loop. |
| 1950 | 12403080 | New data to indicate shared intracellular signaling from leptin and insulin is provided. |
| 1951 | 12403080 | The satiety system for meals, consisting of neural afferents to the hindbrain from the gastrointestinal tract, is described and its effectiveness is shown to vary with the strength of the insulin and leptin signals. |
| 1952 | 12439785 | In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by beta-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. |
| 1953 | 12439785 | Moreover, chelerythrine and GF 109203X diminished the stimulatory action of beta-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). |
| 1954 | 12439785 | In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by beta-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. |
| 1955 | 12439785 | Moreover, chelerythrine and GF 109203X diminished the stimulatory action of beta-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). |
| 1956 | 12442088 | The placenta synthetizes Corticotropin-Releasing Hormone (CRH) and pro-opio-melanocortin (POMC), and the plasma levels of both peptides are highly increased during pregnancy. |
| 1957 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 1958 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 1959 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 1960 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 1961 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 1962 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 1963 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 1964 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 1965 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 1966 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 1967 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 1968 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 1969 | 12453626 | Alpha-melanocyte stimulating hormone suppresses intracerebral tumor necrosis factor-alpha and interleukin-1beta gene expression following transient cerebral ischemia in mice. |
| 1970 | 12453626 | This study's objective was to determine whether the anti-inflammatory neuropeptide alpha-melanocyte stimulating hormone (MSH) can suppress postischemic activation of intracerebral tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) gene expression. |
| 1971 | 12453626 | Ipsilateral TNF-alpha levels were increased in cerebrocortical territory of the middle cerebral artery (MCA) following transient unilateral MCA occlusion (MCAO) and reperfusion in mice, and systemic alpha-MSH treatment (0.5 mg/kg i.p.) suppressed this increase. |
| 1972 | 12453626 | Systemic alpha-MSH treatment also inhibited the marked increases in cortical TNF-alpha and IL-1beta mRNA levels following MCAO, and reduced the intracerebral TNF-alpha protein levels seen after transient global ischemia. |
| 1973 | 12453895 | Compared with lean controls, ob/ob mice had elevated expression of NPY and agouti-related protein (AgRP) mRNA in the arcuate nucleus and decreased expression of proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA. |
| 1974 | 12453895 | Y2 deletion in ob/ob mice significantly increased the hypothalamic POMC mRNA expression, with no effect on NPY, AgRP, or CART expression. |
| 1975 | 12453895 | Compared with lean controls, ob/ob mice had elevated expression of NPY and agouti-related protein (AgRP) mRNA in the arcuate nucleus and decreased expression of proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA. |
| 1976 | 12453895 | Y2 deletion in ob/ob mice significantly increased the hypothalamic POMC mRNA expression, with no effect on NPY, AgRP, or CART expression. |
| 1977 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 1978 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 1979 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 1980 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1981 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 1982 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 1983 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 1984 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 1985 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 1986 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 1987 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 1988 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 1989 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 1990 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 1991 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 1992 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 1993 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 1994 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 1995 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 1996 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 1997 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 1998 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 1999 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 2000 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 2001 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 2002 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 2003 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 2004 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 2005 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 2006 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 2007 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 2008 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 2009 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 2010 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 2011 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 2012 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 2013 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 2014 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 2015 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 2016 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 2017 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 2018 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 2019 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 2020 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 2021 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 2022 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 2023 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 2024 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 2025 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 2026 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 2027 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 2028 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 2029 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 2030 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 2031 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 2032 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 2033 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 2034 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 2035 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 2036 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 2037 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 2038 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 2039 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 2040 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 2041 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 2042 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 2043 | 12488356 | Central administration of neuropeptide Y reduces alpha-melanocyte-stimulating hormone-induced cyclic adenosine 5'-monophosphate response element binding protein (CREB) phosphorylation in pro-thyrotropin-releasing hormone neurons and increases CREB phosphorylation in corticotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus. |
| 2044 | 12488356 | Neuropeptide Y (NPY) has a potent inhibitory effect on TRH gene expression in the paraventricular nucleus (PVN) and contributes to the fall in circulating thyroid hormone levels during fasting mediated by a reduction in serum leptin levels. |
| 2045 | 12488356 | Because alpha-MSH activates the TRH gene by increasing the phosphorylation of CREB in the nucleus of these neurons, we raised the possibility that at least one of the mechanisms by which NPY reduces TRH mRNA in hypophysiotropic neurons is by antagonizing the ability of alpha-MSH to phosphorylate CREB. |
| 2046 | 12488356 | As NPY increases CRH mRNA in the hypothalamus, we further determined whether intracerebroventricular (i.c.v.) administration of NPY regulates the phosphorylation of CREB in hypophysiotropic CRH neurons. |
| 2047 | 12488356 | NPY [10 micro g in artificial CSF (aCSF)] was administered into the lateral ventricle i.c.v. 30 min before the i.c.v. administration of aCSF or alpha-MSH (10 micro g in aCSF), the latter in a dose previously demonstrated to increase proTRH mRNA and phosphorylate CREB in TRH neurons. |
| 2048 | 12488356 | By double-labeling immunocytochemistry, only few TRH neurons in the PVN contained phosphoCREB (PCREB) in animals treated only with aCSF (4 +/- 0.2%) or with NPY followed by aCSF (9.7 +/- 2.5), whereas alpha-MSH-infused animals dramatically increased the percentage of TRH neurons containing PCREB (75.3 +/- 6.9%). |
| 2049 | 12488356 | Pretreatment with NPY before alpha-MSH infusion, however, significantly reduced the percentage of TRH neurons containing PCREB (40.8 +/- 3.5%) compared with alpha-MSH infused animals (P = 0.01). |
| 2050 | 12488356 | Only 12.2 +/- 0.9% of CRH neurons of the medial parvocellular neurons contained PCREB nuclei in vehicle-treated animals, whereas 30 min following NPY infusion, the number of CRH neurons containing PCREB increased dramatically to 88 +/- 2.9%. |
| 2051 | 12488356 | Whereas alpha-MSH infusion increased the percentage of CRH neurons that contained PCREB to 56 +/- 2.2% compared with control, animals pretreated with NPY further increased the number of CRH neurons colocalizing with PCREB to 87 +/- 2.5%. |
| 2052 | 12488356 | These data demonstrate a functional interaction between NPY and alpha-MSH in the regulation of proTRH neurons in the PVN, suggesting that NPY can antagonize alpha-MSH induced activation of the TRH gene by interfering with melanocortin signaling at the postreceptor level, preventing the phosphorylation of CREB. |
| 2053 | 12488356 | In contrast, NPY infusion increases the phosphorylation of CREB in CRH neurons, indicating that NPY has independent effects on discrete populations of neurons in the PVN, presumably mediated through different signaling mechanisms. |
| 2054 | 12499395 | A functional analysis of these mutant receptors, in addition to 11 other childhood obesity-associated MC4R mutations, indicates that they all alter the activation of the receptor by the endogenous agonist alpha-MSH. |
| 2055 | 12553551 | Hypothalamus-pituitary-adrenal axis in central diabetes insipidus: ACTH and cortisol responsiveness to CRH administration. |
| 2056 | 12553551 | The aim of the current study was to evaluate baseline and CRH-stimulated ACTH and F levels in patients with central diabetes insipidus (CDI), before and after replacement therapy with desamino-D-AVP (DDAVP). |
| 2057 | 12553551 | In addition, replacement treatment with DDAVP normalized CRH-induced but not baseline ACTH and F secretion. |
| 2058 | 12553551 | Hypothalamus-pituitary-adrenal axis in central diabetes insipidus: ACTH and cortisol responsiveness to CRH administration. |
| 2059 | 12553551 | The aim of the current study was to evaluate baseline and CRH-stimulated ACTH and F levels in patients with central diabetes insipidus (CDI), before and after replacement therapy with desamino-D-AVP (DDAVP). |
| 2060 | 12553551 | In addition, replacement treatment with DDAVP normalized CRH-induced but not baseline ACTH and F secretion. |
| 2061 | 12553551 | Hypothalamus-pituitary-adrenal axis in central diabetes insipidus: ACTH and cortisol responsiveness to CRH administration. |
| 2062 | 12553551 | The aim of the current study was to evaluate baseline and CRH-stimulated ACTH and F levels in patients with central diabetes insipidus (CDI), before and after replacement therapy with desamino-D-AVP (DDAVP). |
| 2063 | 12553551 | In addition, replacement treatment with DDAVP normalized CRH-induced but not baseline ACTH and F secretion. |
| 2064 | 12606499 | Three more groups underwent pretreatment with corticosterone, adrenocorticotrophic hormone (ACTH), or corticotrophin-releasing hormone (CRH) mirroring the glucocorticoid response of the hypoglycemic group. |
| 2065 | 12606499 | CRH- (and insulin-treated) animals showed markedly reduced epinephrine responses (CRH 1,276 +/- 404 pg/ml, controls 3,559 +/- 563 pg/ml; P < 0.05). |
| 2066 | 12606499 | The addition of a CRH receptor 1 (CRHr1) antagonist to the antecedent CRH reversed the subsequent suppression of epinephrine. |
| 2067 | 12606499 | These findings suggest that CRH acting via CRHr1 plays an important role in the sympathoadrenal downregulation seen in this rodent model of antecedent hypoglycemia; this action is not mediated via activation of the hypothalamic-pituitary-adrenal axis. |
| 2068 | 12639913 | Preexposure of GT1-7 cells that express endogenous MC4R to the agonist for MC4R, alpha-melanocyte-stimulating hormone, resulted in impaired cAMP formation to a second challenge of alpha-melanocyte-stimulating hormone. |
| 2069 | 12639913 | The desensitization of MC4R was accompanied by time-dependent internalization of the receptor in HEK293 cells, which was partly inhibited by pretreatment with a specific protein kinase A (PKA) inhibitor, H89. |
| 2070 | 12639913 | Overexpression of dominant-negative mutants of beta-arrestin1-V53D and dynamin I-K44A prevented agonist-mediated internalization of MC4R. |
| 2071 | 12639913 | Our data demonstrate that, through PKA-, GRK-, beta-arrestin-, and dynamin-dependent processes, MC4R undergoes internalization in response to agonist, thereby providing novel insights into the regulation of MC4R signaling. |
| 2072 | 12654151 | He was followed for more than 15 years and sequentially developed deficiencies of growth hormone, thyroid-stimulating hormone, gonadotrophins and adrenocorticotropic hormone after high-dose cranial irradiation. |
| 2073 | 12660884 | Consumption of a high-fat diet decreases hypothalamic neuropeptide Y (NPY) and increases proopiomelanocortin (POMC) and brown adipose uncoupling protein (UCP)-1 mRNA in obesity-resistant SWR/J but not obesity-prone C57Bl/6J mice. |
| 2074 | 12660884 | Although leptin was elevated in both strains in response to a high-fat diet, its role in the development of diet-induced obesity has remained unclear since insulin and other factors that affect similar tissue targets are altered. |
| 2075 | 12660884 | Sensitivity to fasting in C57Bl/6J mice was associated with higher hypothalamic NPY mRNA and reduced POMC and UCP-1 mRNA expression, while the robust response to high leptin levels in SWR/J mice was associated with suppression of NPY mRNA. |
| 2076 | 12660884 | Consumption of a high-fat diet decreases hypothalamic neuropeptide Y (NPY) and increases proopiomelanocortin (POMC) and brown adipose uncoupling protein (UCP)-1 mRNA in obesity-resistant SWR/J but not obesity-prone C57Bl/6J mice. |
| 2077 | 12660884 | Although leptin was elevated in both strains in response to a high-fat diet, its role in the development of diet-induced obesity has remained unclear since insulin and other factors that affect similar tissue targets are altered. |
| 2078 | 12660884 | Sensitivity to fasting in C57Bl/6J mice was associated with higher hypothalamic NPY mRNA and reduced POMC and UCP-1 mRNA expression, while the robust response to high leptin levels in SWR/J mice was associated with suppression of NPY mRNA. |
| 2079 | 12689472 | Thus noise causes the release of different stress hormones (e.g. corticotropin releasing hormone: CRH; adrenocorticotropic hormone: ACTH) especially in sleeping persons during the vagotropic night/early morning phase. |
| 2080 | 12689472 | Even worse may be the widespread extrahypothalamical effects of CRH/and/or ACTH which have the potential to influence nearly all regulatory systems, causing for example stress-dysmenorrhea etc. as signs of disturbed hormonal balance. |
| 2081 | 12689472 | Thus noise causes the release of different stress hormones (e.g. corticotropin releasing hormone: CRH; adrenocorticotropic hormone: ACTH) especially in sleeping persons during the vagotropic night/early morning phase. |
| 2082 | 12689472 | Even worse may be the widespread extrahypothalamical effects of CRH/and/or ACTH which have the potential to influence nearly all regulatory systems, causing for example stress-dysmenorrhea etc. as signs of disturbed hormonal balance. |
| 2083 | 12717340 | Hyperactivation of the HPA axis in diabetes is associated with increased expression of hypothalamic corticotrophin-releasing hormone (CRH) mRNA and hippocampal mineralocorticoid receptor (MR) mRNA. |
| 2084 | 12717340 | Although insulin replacement restores ACTH and corticosterone levels to normal, likely through glucocorticoid-mediated suppression of ACTH secretion, CRH and MR mRNA expression remain elevated. |
| 2085 | 12727972 | We have synthesized the human N-terminal POMC fragment 1-28-POMC with the disulfide bridges in the correct position between cysteine residues 2-24 and 8-20 and studied the activity of these peptides in adrenocortical tumor cells in vitro. 1-28-POMC stimulated cell proliferation in human NCI-h295 and mouse Y-1 adrenal cancer cell lines and also in primary cultures of bovine adrenocortical cells in a concentration-dependent manner. 1-28-POMC led to rapid activation of the MAPKs extracellular signal-regulated kinases-1 and -2, but not c-Jun N-terminal kinase and p38, pathways. |
| 2086 | 12727972 | However, protein levels of important regulators of steroidogenesis [steroidogenic factor-1, DAX-1 (dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X-chromosome 1), steroidogenic acute regulatory protein, and cytochrome P450 side-chain cleavage enzyme] remained unaffected by 1-28-POMC treatment. |
| 2087 | 12792820 | Hence, we compared the effects of glucagon, glucagon-like peptide (GLP)-1 and GLP-2 on basal and ACTH-stimulated secretion of dispersed adrenocortical cells from normal and STZ-induced diabetic rats. |
| 2088 | 12792820 | In normoglycemic rats, glucagon increased basal aldosterone and corticosterone secretion from ZG and ZF/R cells, GLP-2 raised both basal and ACTH-stimulated aldosterone secretion and ACTH-stimulated corticosterone output, and EX4 increased basal corticosterone secretion. |
| 2089 | 12792820 | It is suggested that the prolonged exposure to low concentrations of insulin causes unresponsiveness of adrenocortical cells to glucagon, GLP-2 and EX4, which may contribute to the hyporeninemic hypoaldosteronism and alterations in glucocorticoid metabolism occurring in experimental diabetes. |
| 2090 | 12792820 | Hence, we compared the effects of glucagon, glucagon-like peptide (GLP)-1 and GLP-2 on basal and ACTH-stimulated secretion of dispersed adrenocortical cells from normal and STZ-induced diabetic rats. |
| 2091 | 12792820 | In normoglycemic rats, glucagon increased basal aldosterone and corticosterone secretion from ZG and ZF/R cells, GLP-2 raised both basal and ACTH-stimulated aldosterone secretion and ACTH-stimulated corticosterone output, and EX4 increased basal corticosterone secretion. |
| 2092 | 12792820 | It is suggested that the prolonged exposure to low concentrations of insulin causes unresponsiveness of adrenocortical cells to glucagon, GLP-2 and EX4, which may contribute to the hyporeninemic hypoaldosteronism and alterations in glucocorticoid metabolism occurring in experimental diabetes. |
| 2093 | 12841938 | Urocortin is a peptide recently identified, structurally related to corticotropin releasing factor (CRF). |
| 2094 | 12841938 | In the arterial segments precontracted with endothelin-1, urocortin produced concentration-dependent relaxation, and the order of sensitivity was: tail > basilar > coronary. |
| 2095 | 12851322 | Two melanocortin receptors (MC3R, MC4R) are expressed in brain regions receiving projections of POMC fibers, most of which also receive projections from a population of ARC neurons that co-express neuropeptide Y (NPY) and the MC3R/MC4R antagonist agouti-related peptide (AgRP). |
| 2096 | 12851322 | The MC4R, but not the MC3R, is required for the stimulation of energy expenditure in response to melanocortin agonists and voluntary hyperphagia. |
| 2097 | 12855418 | Elevated corticosterone and inhibition of ACTH responses to CRH and ether in the neonatal rat: effect of hypoxia from birth. |
| 2098 | 12855418 | At the end of the exposure, plasma ACTH and corticosterone were measured before and after either ether vapors were administered for 3 min or CRH (10 microg/kg) was given intraperitoneally. |
| 2099 | 12855418 | Thyroid function, pituitary pro-opiomelanocortin (POMC) mRNA and ACTH content, and hypothalamic corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and AVP mRNA were also assessed. |
| 2100 | 12855418 | The ACTH responses to ether or CRH administration were almost completely inhibited in hypoxic pups. |
| 2101 | 12855418 | Hypoxia did not affect the established regulators of the neonatal hypothalamic-pituitary-adrenal axis, including pituitary POMC or ACTH content, hypothalamic CRH, NPY, or AVP mRNA (parvo- or magnocellular), or thyroid function. |
| 2102 | 12855418 | Elevated corticosterone and inhibition of ACTH responses to CRH and ether in the neonatal rat: effect of hypoxia from birth. |
| 2103 | 12855418 | At the end of the exposure, plasma ACTH and corticosterone were measured before and after either ether vapors were administered for 3 min or CRH (10 microg/kg) was given intraperitoneally. |
| 2104 | 12855418 | Thyroid function, pituitary pro-opiomelanocortin (POMC) mRNA and ACTH content, and hypothalamic corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and AVP mRNA were also assessed. |
| 2105 | 12855418 | The ACTH responses to ether or CRH administration were almost completely inhibited in hypoxic pups. |
| 2106 | 12855418 | Hypoxia did not affect the established regulators of the neonatal hypothalamic-pituitary-adrenal axis, including pituitary POMC or ACTH content, hypothalamic CRH, NPY, or AVP mRNA (parvo- or magnocellular), or thyroid function. |
| 2107 | 12855418 | Elevated corticosterone and inhibition of ACTH responses to CRH and ether in the neonatal rat: effect of hypoxia from birth. |
| 2108 | 12855418 | At the end of the exposure, plasma ACTH and corticosterone were measured before and after either ether vapors were administered for 3 min or CRH (10 microg/kg) was given intraperitoneally. |
| 2109 | 12855418 | Thyroid function, pituitary pro-opiomelanocortin (POMC) mRNA and ACTH content, and hypothalamic corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and AVP mRNA were also assessed. |
| 2110 | 12855418 | The ACTH responses to ether or CRH administration were almost completely inhibited in hypoxic pups. |
| 2111 | 12855418 | Hypoxia did not affect the established regulators of the neonatal hypothalamic-pituitary-adrenal axis, including pituitary POMC or ACTH content, hypothalamic CRH, NPY, or AVP mRNA (parvo- or magnocellular), or thyroid function. |
| 2112 | 12855418 | Elevated corticosterone and inhibition of ACTH responses to CRH and ether in the neonatal rat: effect of hypoxia from birth. |
| 2113 | 12855418 | At the end of the exposure, plasma ACTH and corticosterone were measured before and after either ether vapors were administered for 3 min or CRH (10 microg/kg) was given intraperitoneally. |
| 2114 | 12855418 | Thyroid function, pituitary pro-opiomelanocortin (POMC) mRNA and ACTH content, and hypothalamic corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and AVP mRNA were also assessed. |
| 2115 | 12855418 | The ACTH responses to ether or CRH administration were almost completely inhibited in hypoxic pups. |
| 2116 | 12855418 | Hypoxia did not affect the established regulators of the neonatal hypothalamic-pituitary-adrenal axis, including pituitary POMC or ACTH content, hypothalamic CRH, NPY, or AVP mRNA (parvo- or magnocellular), or thyroid function. |
| 2117 | 12855418 | Elevated corticosterone and inhibition of ACTH responses to CRH and ether in the neonatal rat: effect of hypoxia from birth. |
| 2118 | 12855418 | At the end of the exposure, plasma ACTH and corticosterone were measured before and after either ether vapors were administered for 3 min or CRH (10 microg/kg) was given intraperitoneally. |
| 2119 | 12855418 | Thyroid function, pituitary pro-opiomelanocortin (POMC) mRNA and ACTH content, and hypothalamic corticotropin-releasing hormone (CRH), neuropeptide Y (NPY), and AVP mRNA were also assessed. |
| 2120 | 12855418 | The ACTH responses to ether or CRH administration were almost completely inhibited in hypoxic pups. |
| 2121 | 12855418 | Hypoxia did not affect the established regulators of the neonatal hypothalamic-pituitary-adrenal axis, including pituitary POMC or ACTH content, hypothalamic CRH, NPY, or AVP mRNA (parvo- or magnocellular), or thyroid function. |
| 2122 | 12882910 | Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats. |
| 2123 | 12882910 | For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. |
| 2124 | 12882910 | Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. |
| 2125 | 12882910 | POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. |
| 2126 | 12882910 | Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. |
| 2127 | 12882910 | This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. |
| 2128 | 12882910 | Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats. |
| 2129 | 12882910 | For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. |
| 2130 | 12882910 | Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. |
| 2131 | 12882910 | POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. |
| 2132 | 12882910 | Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. |
| 2133 | 12882910 | This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. |
| 2134 | 12882910 | Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats. |
| 2135 | 12882910 | For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. |
| 2136 | 12882910 | Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. |
| 2137 | 12882910 | POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. |
| 2138 | 12882910 | Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. |
| 2139 | 12882910 | This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. |
| 2140 | 12882910 | Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats. |
| 2141 | 12882910 | For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. |
| 2142 | 12882910 | Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. |
| 2143 | 12882910 | POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. |
| 2144 | 12882910 | Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. |
| 2145 | 12882910 | This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. |
| 2146 | 12882910 | Central pro-opiomelanocortin gene delivery results in hypophagia, reduced visceral adiposity, and improved insulin sensitivity in genetically obese Zucker rats. |
| 2147 | 12882910 | For testing whether chronic activation of the central melanocortin pathway can bypass the defective leptin signaling and normalize altered energy homeostasis in these rats, recombinant adeno-associated virus encoding pro-opiomelanocortin (rAAV-POMC) or control vector was delivered bilaterally into the basal hypothalamus with coordinates targeting the arcuate nucleus. |
| 2148 | 12882910 | Thirty-eight days after POMC gene delivery, hypothalamic POMC expression increased fourfold and melanocortin signaling (indicated by phosphorylation of CREB) increased by 62% with respect to controls. |
| 2149 | 12882910 | POMC gene delivery enhanced uncoupling protein 1 in brown adipose tissue (BAT) by more than fourfold. |
| 2150 | 12882910 | Fasting serum leptin, insulin, and cholesterol levels were also significantly reduced by rAAV-POMC treatment. |
| 2151 | 12882910 | This study demonstrates that targeted POMC gene delivery in the hypothalamus suppresses food intake and weight gain and reduces visceral adiposity and hyperinsulinemia in leptin-resistant obese Zucker rats. |
| 2152 | 12887368 | Adrenocorticotropin-independent macronodular adrenal hyperplasia treated by simultaneous bilateral laparoscopic adrenalectomy. |
| 2153 | 12887368 | Radiological and endocrinological findings suggested adrenocorticotropic hormone-independent macronodular adrenal hyperplasia. |
| 2154 | 12887368 | Adrenocorticotropin-independent macronodular adrenal hyperplasia treated by simultaneous bilateral laparoscopic adrenalectomy. |
| 2155 | 12887368 | Radiological and endocrinological findings suggested adrenocorticotropic hormone-independent macronodular adrenal hyperplasia. |
| 2156 | 12941772 | Diabetic rats both overeat high-carbohydrate diet and have altered hypothalamic neuropeptide Y (NPY) and corticotropin-releasing factor (CRF). |
| 2157 | 12941772 | In contrast, a high-fat diet reduces caloric intake of diabetics to normal, reflected by normal hypothalamic NPY and CRF content. |
| 2158 | 12965092 | Simultaneously, there was an increase in the mRNAs of the ACTH-receptor and of the steroid-synthesizing enzymes in the fetal adrenal gland of the older, hypoxemic fetuses. |
| 2159 | 12965092 | Growth and maturation of the fetal lung might also have been affected, because of the increase in surfactant-protein A mRNA in the older, hypoxemic animals and the decrease in the insulin-like growth factor-I and its binding protein-5 mRNA in the younger, hypoxemic fetuses. |
| 2160 | 12970157 | Recent work suggests that the melanocortin system is involved in this integration; specifically, central administration of melanocyte-stimulating hormone (MSH) decreases, whereas lack of central MSH signaling increases, peripheral insulin resistance. |
| 2161 | 12970157 | Here we asked whether MSH acting in the periphery has a complementary role in insulin resistance. |
| 2162 | 12970157 | Here we report that homozygous POMC mutants have normal serum levels of insulin, normal fasting levels of glucose, and normal clearance of glucose in glucose tolerance tests. |
| 2163 | 12970157 | However, we found a striking inability of the homozygous POMC mutants to recover from insulin-induced hypoglycemia. |
| 2164 | 12970157 | Both peripheral administration of an MSH analog and supplementation with corticosterone alleviated the hypoglycemia after insulin challenge, but did not make the obese POMC mutant mice diabetic. |
| 2165 | 12970157 | Recent work suggests that the melanocortin system is involved in this integration; specifically, central administration of melanocyte-stimulating hormone (MSH) decreases, whereas lack of central MSH signaling increases, peripheral insulin resistance. |
| 2166 | 12970157 | Here we asked whether MSH acting in the periphery has a complementary role in insulin resistance. |
| 2167 | 12970157 | Here we report that homozygous POMC mutants have normal serum levels of insulin, normal fasting levels of glucose, and normal clearance of glucose in glucose tolerance tests. |
| 2168 | 12970157 | However, we found a striking inability of the homozygous POMC mutants to recover from insulin-induced hypoglycemia. |
| 2169 | 12970157 | Both peripheral administration of an MSH analog and supplementation with corticosterone alleviated the hypoglycemia after insulin challenge, but did not make the obese POMC mutant mice diabetic. |
| 2170 | 12970157 | Recent work suggests that the melanocortin system is involved in this integration; specifically, central administration of melanocyte-stimulating hormone (MSH) decreases, whereas lack of central MSH signaling increases, peripheral insulin resistance. |
| 2171 | 12970157 | Here we asked whether MSH acting in the periphery has a complementary role in insulin resistance. |
| 2172 | 12970157 | Here we report that homozygous POMC mutants have normal serum levels of insulin, normal fasting levels of glucose, and normal clearance of glucose in glucose tolerance tests. |
| 2173 | 12970157 | However, we found a striking inability of the homozygous POMC mutants to recover from insulin-induced hypoglycemia. |
| 2174 | 12970157 | Both peripheral administration of an MSH analog and supplementation with corticosterone alleviated the hypoglycemia after insulin challenge, but did not make the obese POMC mutant mice diabetic. |
| 2175 | 12970157 | Recent work suggests that the melanocortin system is involved in this integration; specifically, central administration of melanocyte-stimulating hormone (MSH) decreases, whereas lack of central MSH signaling increases, peripheral insulin resistance. |
| 2176 | 12970157 | Here we asked whether MSH acting in the periphery has a complementary role in insulin resistance. |
| 2177 | 12970157 | Here we report that homozygous POMC mutants have normal serum levels of insulin, normal fasting levels of glucose, and normal clearance of glucose in glucose tolerance tests. |
| 2178 | 12970157 | However, we found a striking inability of the homozygous POMC mutants to recover from insulin-induced hypoglycemia. |
| 2179 | 12970157 | Both peripheral administration of an MSH analog and supplementation with corticosterone alleviated the hypoglycemia after insulin challenge, but did not make the obese POMC mutant mice diabetic. |
| 2180 | 12970157 | Recent work suggests that the melanocortin system is involved in this integration; specifically, central administration of melanocyte-stimulating hormone (MSH) decreases, whereas lack of central MSH signaling increases, peripheral insulin resistance. |
| 2181 | 12970157 | Here we asked whether MSH acting in the periphery has a complementary role in insulin resistance. |
| 2182 | 12970157 | Here we report that homozygous POMC mutants have normal serum levels of insulin, normal fasting levels of glucose, and normal clearance of glucose in glucose tolerance tests. |
| 2183 | 12970157 | However, we found a striking inability of the homozygous POMC mutants to recover from insulin-induced hypoglycemia. |
| 2184 | 12970157 | Both peripheral administration of an MSH analog and supplementation with corticosterone alleviated the hypoglycemia after insulin challenge, but did not make the obese POMC mutant mice diabetic. |
| 2185 | 13375524 | Comparative studies of alloxan diabetic dog and pancreatectomized diabetic dog on the regulation of the carbohydrate metabolism with special reference to the action of ACTH and adrenocortical hormones on the insulin requirement. |
| 2186 | 13679250 | Leptin stimulates the formation of pro-opiomelanocortin and its products. |
| 2187 | 13679250 | A blood sample was collected and plasma glucose, insulin, leptin, beta-endorphins were measured. |
| 2188 | 13679250 | Leptin and insulin levels were also higher in the HF animals. |
| 2189 | 13679250 | These studies suggest that HF feeding is associated with increased body fat, plasma leptin, insulin, and hypothalamic mu opioid receptors. |
| 2190 | 14557451 | A reappraisal of the utility of somatostatin receptor scintigraphy in patients with ectopic adrenocorticotropin Cushing's syndrome. |
| 2191 | 14557451 | The diagnostic utility of somatostatin receptor scintigraphy (SRS) in EAS has been studied in a limited number of patients with conflicting results. |
| 2192 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2193 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2194 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2195 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2196 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2197 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2198 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2199 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2200 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2201 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2202 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2203 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2204 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2205 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2206 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2207 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2208 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2209 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2210 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2211 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2212 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2213 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2214 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2215 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2216 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2217 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2218 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2219 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2220 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2221 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2222 | 14578285 | Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. |
| 2223 | 14578285 | Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. |
| 2224 | 14578285 | To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. |
| 2225 | 14578285 | Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. |
| 2226 | 14578285 | Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. |
| 2227 | 14578285 | These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging. |
| 2228 | 14599113 | Basal ACTH and DHEA-S levels were significantly lower (p < 0.05 and p < 0.01, respectively), and midnight cortisol and 24-hour urinary free cortisol levels were significantly higher in patients with SCS (p < 0.001 and p < 0.05, respectively). |
| 2229 | 14599113 | Suppressed ACTH and DHEA-S levels, and high midnight cortisol levels may be some clues for SCS in patients with adrenal incidentaloma. |
| 2230 | 14599113 | Basal ACTH and DHEA-S levels were significantly lower (p < 0.05 and p < 0.01, respectively), and midnight cortisol and 24-hour urinary free cortisol levels were significantly higher in patients with SCS (p < 0.001 and p < 0.05, respectively). |
| 2231 | 14599113 | Suppressed ACTH and DHEA-S levels, and high midnight cortisol levels may be some clues for SCS in patients with adrenal incidentaloma. |
| 2232 | 14600075 | Examination of hypothalamic agouti gene-related peptide and proopiomelanocortin mRNA shows normalization of these leptin-regulated transcripts. |
| 2233 | 14601484 | Basal plasma levels of LEP, beta-endorphin (B-EP), cortisol (F), insulin-like growth factor-1 (IGF-1) were measured with RIA test kits. |
| 2234 | 14601484 | Plasma adrenocorticotrophin (ACTH) levels, serum levels of insulin (IRI) and growth hormone (GH) were measured with IRMA test kits. |
| 2235 | 14601484 | Moreover, KON and AD groups demonstrated a negative correlation between plasma ACTH and LEP levels. |
| 2236 | 14601484 | In Addison's disease, downregulation of leptin may reflect an adaptation mechanism to cortisol deficiency and result from low insulin and extremely high adrenocorticotrophin levels. |
| 2237 | 14601484 | In obese subjects, leptin levels may be influenced by cortisol levels, high levels of insulin, IGF-1, and beta-endorphin as well as low levels of growth hormone. |
| 2238 | 14601484 | Basal plasma levels of LEP, beta-endorphin (B-EP), cortisol (F), insulin-like growth factor-1 (IGF-1) were measured with RIA test kits. |
| 2239 | 14601484 | Plasma adrenocorticotrophin (ACTH) levels, serum levels of insulin (IRI) and growth hormone (GH) were measured with IRMA test kits. |
| 2240 | 14601484 | Moreover, KON and AD groups demonstrated a negative correlation between plasma ACTH and LEP levels. |
| 2241 | 14601484 | In Addison's disease, downregulation of leptin may reflect an adaptation mechanism to cortisol deficiency and result from low insulin and extremely high adrenocorticotrophin levels. |
| 2242 | 14601484 | In obese subjects, leptin levels may be influenced by cortisol levels, high levels of insulin, IGF-1, and beta-endorphin as well as low levels of growth hormone. |
| 2243 | 14601484 | Basal plasma levels of LEP, beta-endorphin (B-EP), cortisol (F), insulin-like growth factor-1 (IGF-1) were measured with RIA test kits. |
| 2244 | 14601484 | Plasma adrenocorticotrophin (ACTH) levels, serum levels of insulin (IRI) and growth hormone (GH) were measured with IRMA test kits. |
| 2245 | 14601484 | Moreover, KON and AD groups demonstrated a negative correlation between plasma ACTH and LEP levels. |
| 2246 | 14601484 | In Addison's disease, downregulation of leptin may reflect an adaptation mechanism to cortisol deficiency and result from low insulin and extremely high adrenocorticotrophin levels. |
| 2247 | 14601484 | In obese subjects, leptin levels may be influenced by cortisol levels, high levels of insulin, IGF-1, and beta-endorphin as well as low levels of growth hormone. |
| 2248 | 14601484 | Basal plasma levels of LEP, beta-endorphin (B-EP), cortisol (F), insulin-like growth factor-1 (IGF-1) were measured with RIA test kits. |
| 2249 | 14601484 | Plasma adrenocorticotrophin (ACTH) levels, serum levels of insulin (IRI) and growth hormone (GH) were measured with IRMA test kits. |
| 2250 | 14601484 | Moreover, KON and AD groups demonstrated a negative correlation between plasma ACTH and LEP levels. |
| 2251 | 14601484 | In Addison's disease, downregulation of leptin may reflect an adaptation mechanism to cortisol deficiency and result from low insulin and extremely high adrenocorticotrophin levels. |
| 2252 | 14601484 | In obese subjects, leptin levels may be influenced by cortisol levels, high levels of insulin, IGF-1, and beta-endorphin as well as low levels of growth hormone. |
| 2253 | 14635733 | All 21OHAb positive patients had normal basal cortisol and adrenocorticotropin (ACTH), normal cortisol response after ACTH stimulation, but high plasma renin activity. |
| 2254 | 14653225 | Leptin activates Arc neurons producing alpha-melanocyte-stimulating hormone (alpha-MSH) and inhibits those producing agouti-related protein (AgRP). alpha-MSH is an endogenous agonist for the melanocortin-4 receptor (MC4-R) that is expressed exclusively in the central nervous system (CNS), whereas AgRP acts as a MC4-R antagonist. |
| 2255 | 14671163 | Ghrelin levels correlate with insulin levels, insulin resistance, and high-density lipoprotein cholesterol, but not with gender, menopausal status, or cortisol levels in humans. |
| 2256 | 14671163 | The gut peptide, ghrelin, may participate in the control of energy homeostasis and pituitary hormone secretion in humans, stimulating both food intake and, at pharmacological doses, ACTH and cortisol secretion. |
| 2257 | 14671163 | Therefore, 60 adult men and women of widely varying ages and weights were characterized in terms of body composition and levels of ghrelin, glucose, insulin, lipids, and cortisol. |
| 2258 | 14671163 | Fasting ghrelin levels correlated most strongly with insulin levels (r = -0.39; P = 0.002), insulin resistance as determined by the quantitative insulin sensitivity check index (r = 0.38; P = 0.003), and high-density lipoprotein cholesterol levels (r = 0.33; P = 0.009). |
| 2259 | 14671163 | Meal-induced ghrelin suppression correlated with the postprandial rise in insulin (r = 0.39; P < 0.05). |
| 2260 | 14671163 | Our data are consistent with the hypotheses that insulin may negatively regulate ghrelin and that high-density lipoprotein may be a carrier particle for circulating ghrelin. |
| 2261 | 14686961 | Role of fat amount and type in ameliorating diet-induced obesity: insights at the level of hypothalamic arcuate nucleus leptin receptor, neuropeptide Y and pro-opiomelanocortin mRNA expression. |
| 2262 | 14691009 | To further elucidate the role of proteases capable of cleaving N-terminal proopiomelanocortin (N-POMC)-derived peptides, we have cloned two cDNAs encoding isoforms of the airway trypsin-like protease (AT) from mouse (MAT) and rat (RAT), respectively. |
| 2263 | 14693422 | In cultured adrenocortical cells, SIK1 is rapidly but transiently induced by adrenocorticotropin (ACTH) treatment, suggesting that it contributes to ACTH-mediated induction of steroidogenic enzymes. |
| 2264 | 14693422 | However, ACTH treatment of Y1 mouse adrenocortical cells stimulates a rapid translocation of SIK1 from the nucleus to the cytoplasm, and SIK1 represses the transcription of a steroidogenic enzyme by inhibiting the action of cAMP-responsive elements in the promoter. |
| 2265 | 14693422 | SIK2 is found in adipocytes and phosphorylates a specific serine residue in insulin receptor substrate-1. |
| 2266 | 14693422 | Thus, members of the SIK family are emerging as important modulators of key processes such as steroid hormone biosynthesis by the adrenal cortex and insulin signaling in adipocytes. |
| 2267 | 14693422 | In cultured adrenocortical cells, SIK1 is rapidly but transiently induced by adrenocorticotropin (ACTH) treatment, suggesting that it contributes to ACTH-mediated induction of steroidogenic enzymes. |
| 2268 | 14693422 | However, ACTH treatment of Y1 mouse adrenocortical cells stimulates a rapid translocation of SIK1 from the nucleus to the cytoplasm, and SIK1 represses the transcription of a steroidogenic enzyme by inhibiting the action of cAMP-responsive elements in the promoter. |
| 2269 | 14693422 | SIK2 is found in adipocytes and phosphorylates a specific serine residue in insulin receptor substrate-1. |
| 2270 | 14693422 | Thus, members of the SIK family are emerging as important modulators of key processes such as steroid hormone biosynthesis by the adrenal cortex and insulin signaling in adipocytes. |
| 2271 | 14700749 | Tumor galanin and ACTH contents were closely correlated in all tumors. |
| 2272 | 14700749 | In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations. |
| 2273 | 14700749 | Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus. |
| 2274 | 14700749 | Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population. |
| 2275 | 14700749 | Tumor galanin and ACTH contents were closely correlated in all tumors. |
| 2276 | 14700749 | In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations. |
| 2277 | 14700749 | Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus. |
| 2278 | 14700749 | Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population. |
| 2279 | 14700749 | Tumor galanin and ACTH contents were closely correlated in all tumors. |
| 2280 | 14700749 | In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations. |
| 2281 | 14700749 | Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus. |
| 2282 | 14700749 | Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population. |
| 2283 | 14700749 | Tumor galanin and ACTH contents were closely correlated in all tumors. |
| 2284 | 14700749 | In some tumors galanin mRNA and POMC levels coexisted, in others they were essentially in different cell populations. |
| 2285 | 14700749 | Corticotrophin releasing hormone injections in two patients caused ACTH, but no detectable galanin release into sinus petrosus. |
| 2286 | 14700749 | Our results demonstrate that corticotroph, but not GH adenomas, express high levels of galanin, in addition to ACTH, and that in some tumors both polypeptides are synthesised in the same cell population. |
| 2287 | 14709154 | It has previously been suggested that ACTH and ACTH-related peptides may act as paracrine modulators of insulin secretion in the islets of Langerhans. |
| 2288 | 14709154 | Two inhibitors of the protein kinase A (PKA) signaling pathway, Rp-cAMPS (500 microM) and H-89 (10 microM), abolished the insulin secretory response to ACTH(1-24) (0.5-10 nM). |
| 2289 | 14709154 | Overall the results demonstrate that the MC2-R is expressed in beta-cells and suggest that activation of the receptor by ACTH initiates insulin secretion through the activation of PKA in association with Ca2+ influx into beta-cells. |
| 2290 | 14711793 | At early time points, we measured organ histology, leukocyte accumulation, myeloperoxidase activity, activation of nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, in addition to messenger RNA for intracellular adhesion molecule-1 and tumor necrosis factor-alpha. |
| 2291 | 14711793 | Renal ischemia rapidly activated kidney and lung nuclear factor-kappaB, p38 mitogen-activated protein kinase, c-Jun, and activator protein-1 pathways, and distant lung injury. |
| 2292 | 14711793 | Alpha-MSH administration immediately before reperfusion significantly decreased kidney and lung injury and prevented activation of kidney and lung transcription factors and stress response genes, and lung intracellular adhesion molecule-1 and tumor necrosis factor-alpha at early time points after renal ischemia/reperfusion. |
| 2293 | 14724732 | These are fatty acid-binding protein 2 (FABP2), FABP4, and FABP5 for Olep1, and proopiomelanocortin (POMC) and glucose regulatory protein (GCKR) for Olep2. |
| 2294 | 14749508 | Regulation of the pro-opiomelanocortin (pomc) and the thyrotropin-releasing hormone (trh) genes by leptin is particularly well understood. |
| 2295 | 14988462 | In the ARC, orexigenic neuropeptides such as neuropeptide Y (NPY), galanin (GAL), and agouti-related peptide (AGRP) and anorexigenic neuropeptides such as proopiomelanocortin (POMC) and alpha-melanocyte-stimulating hormone (MSH) are expressed. |
| 2296 | 14988462 | The ARC of CO-GD rats showed increased immunopositivity of both NPY and AGRP under basal conditions, despite normal levels of glucose, leptin, and insulin. |
| 2297 | 15001431 | Followup during the suckling, postsuckling, and adult stages (7-120 days of age) revealed hypoleptinemia in males and females, and hypoinsulinemia, a relative increase in the glucose-to-insulin ratio, and a larger increase in skeletal muscle glucose transporter (GLUT 4) concentrations predominantly in the males, reflective of a catabolic state associated with a persistent decrease in body weight gain. |
| 2298 | 15001431 | In addition, the changes in the hormonal/metabolic milieu were associated with an increase in hypothalamic neuropeptide Y content in males and females during the suckling phase, which persisted only in the 120-day-old female with a transient postnatal decline in alpha-melanocyte-stimulating hormone and corticotropin-releasing factor. |
| 2299 | 15003481 | Further studies revealed not only resistance of plasma concentrations of cortisol, adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) to suppression by a low dose of dexamethasone, but also elevated plasma concentrations of growth hormone (GH) and insulin-like growth factor I (IGF-I). |
| 2300 | 15070774 | Signal transducer and activator of transcription (STAT)3 is widely expressed in the CNS during development and adulthood. |
| 2301 | 15070774 | STAT3 has been implicated in the control of neuron/glial differentiation and leptin-mediated energy homeostasis, but the physiological role and degree of involvement of STAT3 in these processes is not defined and controversial because of the lack of a direct genetic model. |
| 2302 | 15070774 | Administering a melanocortin-3/4 receptor agonist abrogated the hyperphagia and hypothalamic immunohistochemistry showed a marked reduction in proopiomelanocortin with an increase in neuropeptide Y and agouti-related protein. |
| 2303 | 15070774 | STAT3(N-/-) mice are hyperleptinemic, suggesting a leptin-resistant condition. |
| 2304 | 15070935 | Low- and standard-dose corticotropin and insulin hypoglycemia testing in the assessment of hypothalamic-pituitary-adrenal function after pituitary surgery. |
| 2305 | 15070935 | We compared low-dose (1 micro g iv) and standard-dose (250 micro g im) corticotropin tests performed 1 and 4-6 wk after pituitary surgery with an insulin hypoglycemia test performed at 4-6 wk. |
| 2306 | 15070935 | Low- and standard-dose corticotropin and insulin hypoglycemia testing in the assessment of hypothalamic-pituitary-adrenal function after pituitary surgery. |
| 2307 | 15070935 | We compared low-dose (1 micro g iv) and standard-dose (250 micro g im) corticotropin tests performed 1 and 4-6 wk after pituitary surgery with an insulin hypoglycemia test performed at 4-6 wk. |
| 2308 | 15093691 | In addition, hypothalamic expression of orexigenic neuropeptide Y and agouti-related peptide mRNA levels was upregulated while the anorexigenic cocaine and amphetamine regulated transcript and proopiomelanocortin mRNA levels were reduced. |
| 2309 | 15111491 | These impaired responses were associated with the destruction of 3v tanycytes, reduced glial fibrillary acidic protein-immunoreactivity surrounding the 3v, neuronal swelling, and decreased arcuate nucleus neuropeptide Y (NPY) mRNA. |
| 2310 | 15111491 | At this time there were significant decreases in GK, NPY, and proopiomelanocortin mRNA. |
| 2311 | 15128476 | Primary aldosteronism, congenital adrenal hyperplasia, Cushing's syndrome, glucocorticoid-remediable aldosteronism, and corticotropin-dependent forms of adrenal pathology can cause hypertension by excessive production of adrenocortical hormones. |
| 2312 | 15133294 | The results showed that the radon and thermal therapy enhanced the antioxidation functions, such as the activities of superoxide dismutase (SOD) and catalase, which inhibit lipid peroxidation and total cholesterol produced in the body. |
| 2313 | 15133294 | Moreover the therapy enhanced concanavalin A (ConA)-induced mitogen response and increased the percentage of CD4 positive cells, which is the marker of helper T cells, and decreased the percentage of CD8 positive cells, which is the common marker of killer T cells and suppressor T cells, in the white blood cell differentiation antigen (CD8/CD4) assay. |
| 2314 | 15133294 | Furthermore, the therapy increased the levels of alpha atrial natriuretic polypeptide (alpha ANP), beta endorphin, adrenocorticotropic hormone (ACTH), insulin and glucose-6-phosphate dehydrogenase (G-6-PDH), and it decreased the vasopression level. |
| 2315 | 15240363 | Acutely, glucocorticoids act to inhibit stress-induced corticotrophin-releasing factor (CRF) and adrenocorticotrophic hormone (ACTH) secretion through their actions in brain and anterior pituitary (canonical feedback). |
| 2316 | 15240363 | Infusion of corticosterone intracerebroventricularly into adrenalectomized rats increases basal ACTH, tends to increase CRF, and allows facilitation of ACTH responses to repeated restraint. |
| 2317 | 15240363 | Increased energy stores feedback on brain to inhibit hypothalamic CRF and decrease the expression of dopamine-beta-hydroxylase in the locus coeruleus. |
| 2318 | 15240363 | Acutely, glucocorticoids act to inhibit stress-induced corticotrophin-releasing factor (CRF) and adrenocorticotrophic hormone (ACTH) secretion through their actions in brain and anterior pituitary (canonical feedback). |
| 2319 | 15240363 | Infusion of corticosterone intracerebroventricularly into adrenalectomized rats increases basal ACTH, tends to increase CRF, and allows facilitation of ACTH responses to repeated restraint. |
| 2320 | 15240363 | Increased energy stores feedback on brain to inhibit hypothalamic CRF and decrease the expression of dopamine-beta-hydroxylase in the locus coeruleus. |
| 2321 | 15277371 | Peptide YY(3-36) (PYY(3-36)) is released by the gut in response to nutrient ingestion. |
| 2322 | 15277371 | It modulates the activities of orexigenic neuropeptide Y (NPY) neurons and anorexigenic proopiomelanocortin (POMC) neurons in the hypothalamus to inhibit food intake. |
| 2323 | 15277371 | Because both NPY and POMC have also been shown to impact insulin action, we wondered whether PYY(3-36) could improve insulin sensitivity. |
| 2324 | 15277371 | In contrast, PYY(3-36) did not impact insulin action on endogenous glucose production or FFA metabolism. |
| 2325 | 15277371 | These data indicate that PYY(3-36) reinforces insulin action on glucose disposal in mice fed a high-fat diet, through a mechanism that is independent of food intake and body weight. |
| 2326 | 15277371 | Peptide YY(3-36) (PYY(3-36)) is released by the gut in response to nutrient ingestion. |
| 2327 | 15277371 | It modulates the activities of orexigenic neuropeptide Y (NPY) neurons and anorexigenic proopiomelanocortin (POMC) neurons in the hypothalamus to inhibit food intake. |
| 2328 | 15277371 | Because both NPY and POMC have also been shown to impact insulin action, we wondered whether PYY(3-36) could improve insulin sensitivity. |
| 2329 | 15277371 | In contrast, PYY(3-36) did not impact insulin action on endogenous glucose production or FFA metabolism. |
| 2330 | 15277371 | These data indicate that PYY(3-36) reinforces insulin action on glucose disposal in mice fed a high-fat diet, through a mechanism that is independent of food intake and body weight. |
| 2331 | 15277373 | Neuropeptide Y (NPY) inhibited and alpha-melanocyte-stimulating hormone stimulated ARC glucose-excited neurons. |
| 2332 | 15292297 | Immunohistochemically, in contrast to primary tumor and first relapse, we found strong immunostaining for ACTH in tumor cells of the second relapse and a MIB-1 index greater than 20%. |
| 2333 | 15322334 | Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat. |
| 2334 | 15322334 | Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. |
| 2335 | 15322334 | In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. |
| 2336 | 15322334 | Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. |
| 2337 | 15322334 | Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations. |
| 2338 | 15322334 | Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat. |
| 2339 | 15322334 | Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. |
| 2340 | 15322334 | In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. |
| 2341 | 15322334 | Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. |
| 2342 | 15322334 | Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations. |
| 2343 | 15322334 | Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat. |
| 2344 | 15322334 | Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. |
| 2345 | 15322334 | In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. |
| 2346 | 15322334 | Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. |
| 2347 | 15322334 | Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations. |
| 2348 | 15322334 | Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat. |
| 2349 | 15322334 | Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. |
| 2350 | 15322334 | In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. |
| 2351 | 15322334 | Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. |
| 2352 | 15322334 | Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations. |
| 2353 | 15322334 | Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat. |
| 2354 | 15322334 | Selenium deficiency did not affect basal and short-term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. |
| 2355 | 15322334 | In contrast, after long-term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. |
| 2356 | 15322334 | Plasma leptin concentrations were 50% lower in Se- compared to Se+ animals following long-term ACTH. |
| 2357 | 15322334 | Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations. |
| 2358 | 15372367 | Mutation analysis of leukemia inhibitory factor-receptor (LIF-R) in ACTH-secreting pituitary adenomas. |
| 2359 | 15372367 | LIF and its receptor LIF-R are abundantly expressed in normal pituitaries and in ACTH producing adenomas. |
| 2360 | 15386812 | Mediation of beta-endorphin in exercise-induced improvement in insulin resistance in obese Zucker rats. |
| 2361 | 15472174 | An insertional polymorphism of the proopiomelanocortin gene is associated with fasting insulin levels in childhood obesity. |
| 2362 | 15472174 | The aim of this study was to investigate the influence of proopiomelanocortin (POMC) in the variability of insulin levels in early-onset obesity. |
| 2363 | 15472174 | An insertional polymorphism of the proopiomelanocortin gene is associated with fasting insulin levels in childhood obesity. |
| 2364 | 15472174 | The aim of this study was to investigate the influence of proopiomelanocortin (POMC) in the variability of insulin levels in early-onset obesity. |
| 2365 | 15481810 | These so-called hypophysiotropic neurons are under feedback inhibition by circulating levels of thyroid hormone, mediated through interactions with the beta2 thyroid hormone receptor (TRbeta2) and competition with the phosphorylated form of cyclic adenosine 5'-monophosphate response element binding protein (CREB) for a multifunctional binding site in the TRH gene. |
| 2366 | 15481810 | These factors include alpha melanocyte-stimulating hormone (alphaMSH) and cocaine- and amphetamine-regulated transcript (CART), and agouti-related protein (AGRP) and neuropeptide Y (NPY), substances co-produced by distinct populations of leptin-responsive neurons in the hypothalamic arcuate nucleus. |
| 2367 | 15494609 | Hippocampal glucocorticoid receptor (GR), hypothalamic paraventricular nucleus (PVN) GR and corticotropin-releasing hormone (CRH), and pituitary GR and proopiomelanocortin (POMC) mRNA levels did not differ. |
| 2368 | 15494609 | We conclude that blunted corticosterone responses to hypoglycemia in diabetic rats are not due to altered basal expression of GR, CRH, and POMC in the hippocampus, PVN, and pituitary. |
| 2369 | 15494609 | Hippocampal glucocorticoid receptor (GR), hypothalamic paraventricular nucleus (PVN) GR and corticotropin-releasing hormone (CRH), and pituitary GR and proopiomelanocortin (POMC) mRNA levels did not differ. |
| 2370 | 15494609 | We conclude that blunted corticosterone responses to hypoglycemia in diabetic rats are not due to altered basal expression of GR, CRH, and POMC in the hippocampus, PVN, and pituitary. |
| 2371 | 15505757 | Medical history, physical examination, and basal levels of free testosterone (fT), androstenedione, follicle-stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone-sulphate (DHEAS), 17 hydroxyprogesterone (17-OHP), 11-deoxycortisol (11-S), thyroid hormones, thyroid stimulating hormone (TSH), and prolactin were determined. |
| 2372 | 15505757 | ACTH stimulation test was performed for the diagnosis of non-classic congenital adrenal hyperplasia (NCAH). |
| 2373 | 15522996 | Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia. |
| 2374 | 15522996 | Resistin is an adipocyte-secreted hormone proposed to link obesity with insulin resistance and diabetes, but no previous study has performed a joint quantitative evaluation of white adipose tissue (WAT) resistin mRNA expression and serum levels in relation to insulinemia and glycemia in mice. |
| 2375 | 15522996 | We have thus comparatively assessed WAT resistin mRNA expression and serum resistin levels in lean C57BL/6J mice and various mouse models of obesity, including diet-induced obese (DIO) C57BL/6J mice, high fat-fed TNF-alpha-/- mice, and brown adipose tissue (BAT)-deficient uncoupling protein-diphtheria toxin A chain (UCP1-DTA) mice. |
| 2376 | 15522996 | We also studied whether treatment with the weight-reducing and insulin-sensitizing compounds, MTII, an alpha-melanocyte-stimulating hormone analog, or CNTF(Ax15), a ciliary neurotrophic factor analog, alters resistin mRNA expression and/or circulating levels in lean and DIO C57BL/6J mice. |
| 2377 | 15522996 | We find that resistin mRNA expression is similar in DIO and lean C57BL/6J mice, as well as in TNF-alpha-/- and wild-type (WT) mice. |
| 2378 | 15522996 | Circulating resistin levels, however, are higher in DIO C57BL/6J, high fat-fed TNF-alpha-/-, and UCP1-DTA mice compared with lean controls. |
| 2379 | 15522996 | Moreover, although resistin mRNA expression is upregulated by MTII treatment for 24 h and downregulated by CNTF(Ax15) treatment for 3 or 7 days, circulating resistin levels are not altered by MTII or CNTF(Ax15) treatment. |
| 2380 | 15522996 | In addition, serum resistin levels, but not resistin mRNA expression levels, are correlated with body weight, and neither resistin mRNA expression nor serum resistin levels are correlated with serum insulin or glucose levels. |
| 2381 | 15522996 | We conclude that transcriptional regulation of resistin in WAT does not correlate with circulating resistin levels and that circulating resistin is unlikely to play a major endocrine role in insulin resistance or glycemia in mice. |
| 2382 | 15525585 | Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake. |
| 2383 | 15525585 | The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. |
| 2384 | 15525585 | Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. |
| 2385 | 15525585 | Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. |
| 2386 | 15525585 | However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. |
| 2387 | 15525585 | Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. |
| 2388 | 15525585 | Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. |
| 2389 | 15525585 | Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake. |
| 2390 | 15525585 | The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. |
| 2391 | 15525585 | Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. |
| 2392 | 15525585 | Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. |
| 2393 | 15525585 | However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. |
| 2394 | 15525585 | Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. |
| 2395 | 15525585 | Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. |
| 2396 | 15525585 | Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake. |
| 2397 | 15525585 | The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. |
| 2398 | 15525585 | Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. |
| 2399 | 15525585 | Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. |
| 2400 | 15525585 | However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. |
| 2401 | 15525585 | Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. |
| 2402 | 15525585 | Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. |
| 2403 | 15525585 | Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake. |
| 2404 | 15525585 | The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. |
| 2405 | 15525585 | Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. |
| 2406 | 15525585 | Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. |
| 2407 | 15525585 | However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. |
| 2408 | 15525585 | Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. |
| 2409 | 15525585 | Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. |
| 2410 | 15525585 | Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake. |
| 2411 | 15525585 | The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. |
| 2412 | 15525585 | Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. |
| 2413 | 15525585 | Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. |
| 2414 | 15525585 | However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. |
| 2415 | 15525585 | Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. |
| 2416 | 15525585 | Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. |
| 2417 | 15579751 | Identification of patients with Cushing's disease with negative pituitary adrenocorticotropin gradients during inferior petrosal sinus sampling: prolactin as an index of pituitary venous effluent. |
| 2418 | 15579751 | The IPS:P ACTH ratio normalized to IPS:P PRL was greater than 0.8 in all CD patients but was less than 0.6 in EAS patients. |
| 2419 | 15579751 | The IPS:P ACTH ratios normalized to IPS:P PRL were greater than 1.2 in the index cases, which was similar to those with CD. |
| 2420 | 15579751 | Identification of patients with Cushing's disease with negative pituitary adrenocorticotropin gradients during inferior petrosal sinus sampling: prolactin as an index of pituitary venous effluent. |
| 2421 | 15579751 | The IPS:P ACTH ratio normalized to IPS:P PRL was greater than 0.8 in all CD patients but was less than 0.6 in EAS patients. |
| 2422 | 15579751 | The IPS:P ACTH ratios normalized to IPS:P PRL were greater than 1.2 in the index cases, which was similar to those with CD. |
| 2423 | 15579751 | Identification of patients with Cushing's disease with negative pituitary adrenocorticotropin gradients during inferior petrosal sinus sampling: prolactin as an index of pituitary venous effluent. |
| 2424 | 15579751 | The IPS:P ACTH ratio normalized to IPS:P PRL was greater than 0.8 in all CD patients but was less than 0.6 in EAS patients. |
| 2425 | 15579751 | The IPS:P ACTH ratios normalized to IPS:P PRL were greater than 1.2 in the index cases, which was similar to those with CD. |
| 2426 | 15627023 | On tapering, one should be aware of the possible development of corticosteroid dependency or withdrawal effects.Novel therapies include vascular endothelial growth factor receptor inhibitors and corticotropin releasing factor, which should undergo further clinical testing before they can be recommended in practice. |
| 2427 | 15649453 | Orexigenic neuropeptides, like neuropeptide Y (NPY) and agouti-related peptide (AGRP), and anorexigenic neuropeptides, like proopiomelanocortin (POMC) and alpha-melanocyte-stimulating hormone (MSH), are decisively involved in body weight regulation. |
| 2428 | 15649453 | Despite of normal leptin and insulin levels in TSGD offspring, increased immunopositivity of NPY and AGRP appeared. |
| 2429 | 15662598 | The diagnosis is usually established by clinical examination and analysis of serum hormone levels (adrenocorticotropin hormone [ACTH], cortisol, thyroid stimulating hormone [TSH], triiodothyronine [fT3], thyroxine [fT4]). |
| 2430 | 15774766 | Basal: Elevated basal ACTH and corticosterone in STZ rats were normalized with insulin but not phloridzin. |
| 2431 | 15774766 | Increases in hypothalamic corticotrophin-releasing hormone (CRH) and inhibitory hippocampal mineralocorticoid receptor (MR) mRNA with STZ diabetes were not restored with either insulin or phloridzin treatments. |
| 2432 | 15774766 | Insulin and phloridzin restored both ACTH and corticosterone responses in diabetic animals. |
| 2433 | 15774766 | Hypothalamic CRH mRNA and pituitary pro-opiomelanocortin mRNA expression increased following 2 h of hypoglycemia in normal, insulin-treated, and phloridzin-treated diabetic rats but not in untreated diabetic rats. |
| 2434 | 15774766 | Interestingly, hypoglycemia decreased hippocampal MR mRNA in control, insulin-, and phloridzin-treated diabetic rats but not uncontrolled diabetic rats, whereas glucocorticoid receptor mRNA was not altered by hypoglycemia. |
| 2435 | 15774766 | Basal: Elevated basal ACTH and corticosterone in STZ rats were normalized with insulin but not phloridzin. |
| 2436 | 15774766 | Increases in hypothalamic corticotrophin-releasing hormone (CRH) and inhibitory hippocampal mineralocorticoid receptor (MR) mRNA with STZ diabetes were not restored with either insulin or phloridzin treatments. |
| 2437 | 15774766 | Insulin and phloridzin restored both ACTH and corticosterone responses in diabetic animals. |
| 2438 | 15774766 | Hypothalamic CRH mRNA and pituitary pro-opiomelanocortin mRNA expression increased following 2 h of hypoglycemia in normal, insulin-treated, and phloridzin-treated diabetic rats but not in untreated diabetic rats. |
| 2439 | 15774766 | Interestingly, hypoglycemia decreased hippocampal MR mRNA in control, insulin-, and phloridzin-treated diabetic rats but not uncontrolled diabetic rats, whereas glucocorticoid receptor mRNA was not altered by hypoglycemia. |
| 2440 | 15774766 | Basal: Elevated basal ACTH and corticosterone in STZ rats were normalized with insulin but not phloridzin. |
| 2441 | 15774766 | Increases in hypothalamic corticotrophin-releasing hormone (CRH) and inhibitory hippocampal mineralocorticoid receptor (MR) mRNA with STZ diabetes were not restored with either insulin or phloridzin treatments. |
| 2442 | 15774766 | Insulin and phloridzin restored both ACTH and corticosterone responses in diabetic animals. |
| 2443 | 15774766 | Hypothalamic CRH mRNA and pituitary pro-opiomelanocortin mRNA expression increased following 2 h of hypoglycemia in normal, insulin-treated, and phloridzin-treated diabetic rats but not in untreated diabetic rats. |
| 2444 | 15774766 | Interestingly, hypoglycemia decreased hippocampal MR mRNA in control, insulin-, and phloridzin-treated diabetic rats but not uncontrolled diabetic rats, whereas glucocorticoid receptor mRNA was not altered by hypoglycemia. |
| 2445 | 15829786 | Five years after traumatic brain injury, repeat neuroendocrine assessment, prompted by an increasing serum insulin-like growth factor-1 level, showed normal growth hormone and adrenocorticotropin hormone responses. |
| 2446 | 15841180 | We generated mice lacking Irs2 in beta cells and a population of hypothalamic neurons (RIPCreIrs2KO), in all neurons (NesCreIrs2KO), and in proopiomelanocortin neurons (POMCCreIrs2KO) to determine the role of Irs2 in the CNS and beta cell. |
| 2447 | 15841180 | RIPCreIrs2KO and NesCreIrs2KO mice retained leptin sensitivity, which suggests that CNS Irs2 pathways are not required for leptin action. |
| 2448 | 15841180 | RIPCre neurons did not express POMC or neuropeptide Y. |
| 2449 | 15841180 | Insulin and a melanocortin agonist depolarized RIPCre neurons, whereas leptin was ineffective. |
| 2450 | 15841180 | Insulin hyperpolarized and leptin depolarized POMC neurons. |
| 2451 | 15841180 | We generated mice lacking Irs2 in beta cells and a population of hypothalamic neurons (RIPCreIrs2KO), in all neurons (NesCreIrs2KO), and in proopiomelanocortin neurons (POMCCreIrs2KO) to determine the role of Irs2 in the CNS and beta cell. |
| 2452 | 15841180 | RIPCreIrs2KO and NesCreIrs2KO mice retained leptin sensitivity, which suggests that CNS Irs2 pathways are not required for leptin action. |
| 2453 | 15841180 | RIPCre neurons did not express POMC or neuropeptide Y. |
| 2454 | 15841180 | Insulin and a melanocortin agonist depolarized RIPCre neurons, whereas leptin was ineffective. |
| 2455 | 15841180 | Insulin hyperpolarized and leptin depolarized POMC neurons. |
| 2456 | 15841180 | We generated mice lacking Irs2 in beta cells and a population of hypothalamic neurons (RIPCreIrs2KO), in all neurons (NesCreIrs2KO), and in proopiomelanocortin neurons (POMCCreIrs2KO) to determine the role of Irs2 in the CNS and beta cell. |
| 2457 | 15841180 | RIPCreIrs2KO and NesCreIrs2KO mice retained leptin sensitivity, which suggests that CNS Irs2 pathways are not required for leptin action. |
| 2458 | 15841180 | RIPCre neurons did not express POMC or neuropeptide Y. |
| 2459 | 15841180 | Insulin and a melanocortin agonist depolarized RIPCre neurons, whereas leptin was ineffective. |
| 2460 | 15841180 | Insulin hyperpolarized and leptin depolarized POMC neurons. |
| 2461 | 15870911 | Urocortin, a recently identified member of the corticotropin-releasing factor (CRF) family, is implicated in the central control of appetite and energy metabolism. |
| 2462 | 15870911 | Urocortin decreased food intake and body weight gain more potently than CRF. |
| 2463 | 15926921 | Hypothalamic anorexigenic [corticotropin-releasing factor (CRF) and proopiomelanocortin] peptides decrease and the orexigen, neuropeptide Y, increases with diabetic hyperphagia. |
| 2464 | 16081264 | Plasma was analyzed for glucose, triglycerides, parameters of renal function and peptide hormones -- insulin, leptin, glucagon and ACTH -- that are involved in glucose and lipid metabolism. |
| 2465 | 16081264 | Isoflavones had significant effect on plasma insulin, leptin and glucagon in lean rats but not in obese rats. |
| 2466 | 16157982 | The patient showed exaggerated adrenocorticotropic hormone responsiveness as determined by a corticotrophin releasing hormone test and elevated serum leptin concentrations associated with ravenous appetite and insulin resistance mediated in part through disturbances in leptin signaling. |
| 2467 | 16181081 | Low levels of neuropeptide Y, somatostatin and corticotropin-releasing factor, described in Alzheimer disease (AD), were related to a defect in proteolytic processing of their protein precursors. |
| 2468 | 16195775 | Small-cell lung cancer presenting with a combination of cranial diabetes insipidus and Cushing's syndrome secondary to ectopic adrenocorticotropin (ACTH) secretion is very rare and has only been described previously in one case report Our patient was a 49 year old man, in whom the initial presenting features of small-cell lung cancer were cranial diabetes insipidus secondary to pituitary metastases and severe hypokalaemia resulting from ectopic ACTH hormone secretion. |
| 2469 | 16202863 | Her plasma ACTH levels were also elevated (>300 pg/mL) and irresponsive to corticotropin-releasing hormone (CRH) or metyrapone administration. |
| 2470 | 16202863 | Subsequent histologic evaluation of the transected paranglioma tissue revealed ACTH, synaptin, and chromogranin-A histologically immunostaining. |
| 2471 | 16202863 | Her plasma ACTH levels were also elevated (>300 pg/mL) and irresponsive to corticotropin-releasing hormone (CRH) or metyrapone administration. |
| 2472 | 16202863 | Subsequent histologic evaluation of the transected paranglioma tissue revealed ACTH, synaptin, and chromogranin-A histologically immunostaining. |
| 2473 | 16203117 | Injection of myricetin three times daily for three consecutive days resulted in increased expression of the glucose transporter subtype 4 (GLUT 4) in soleus muscle and in reduced expression of phosphoenolpyruvate carboxykinase (PEPCK) in liver; these inductions were preventable by opioid mu-receptor blockade. |
| 2474 | 16203117 | Findings support the conclusion that the plasma glucose-lowering action of myricetin in insulin-deficient animals is mediated by activation of opioid mu-receptors of peripheral tissues in response to increased beta-endorphin secretion. |
| 2475 | 16203117 | Opioid mu-receptor activation is held responsible for the enhancement of muscle GLUT 4 gene expression and the attenuation of hepatic PEPCK gene expression observed in these myricetin-treated diabetic animals. |
| 2476 | 16210367 | Differential effects of central leptin, insulin, or glucose administration during fasting on the hypothalamic-pituitary-thyroid axis and feeding-related neurons in the arcuate nucleus. |
| 2477 | 16210367 | The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript. |
| 2478 | 16210367 | Because the central administration of leptin is capable of preventing the inhibitory effects of fasting on TRH mRNA in hypophysiotropic neurons primarily through effects on the arcuate nucleus, we determined whether the continuous administration of 30 mU/d insulin or 648 microg/d glucose into the cerebrospinal fluid by osmotic minipump might also have similar effects on the hypothalamic-pituitary-thyroid axis. |
| 2479 | 16210367 | As anticipated, the intracerebroventricular infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased proopiomelanocortin and cocaine and amphetamine-regulated transcript mRNA in the arcuate nucleus. |
| 2480 | 16210367 | In contrast, whereas insulin increased proopiomelanocortin mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA or circulating thyroid hormone levels. |
| 2481 | 16210367 | We conclude that insulin and glucose only partially replicate the central effects of leptin and may not be essential components of the hypothalamic-pituitary-thyroid regulatory system during fasting. |
| 2482 | 16210367 | Differential effects of central leptin, insulin, or glucose administration during fasting on the hypothalamic-pituitary-thyroid axis and feeding-related neurons in the arcuate nucleus. |
| 2483 | 16210367 | The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript. |
| 2484 | 16210367 | Because the central administration of leptin is capable of preventing the inhibitory effects of fasting on TRH mRNA in hypophysiotropic neurons primarily through effects on the arcuate nucleus, we determined whether the continuous administration of 30 mU/d insulin or 648 microg/d glucose into the cerebrospinal fluid by osmotic minipump might also have similar effects on the hypothalamic-pituitary-thyroid axis. |
| 2485 | 16210367 | As anticipated, the intracerebroventricular infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased proopiomelanocortin and cocaine and amphetamine-regulated transcript mRNA in the arcuate nucleus. |
| 2486 | 16210367 | In contrast, whereas insulin increased proopiomelanocortin mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA or circulating thyroid hormone levels. |
| 2487 | 16210367 | We conclude that insulin and glucose only partially replicate the central effects of leptin and may not be essential components of the hypothalamic-pituitary-thyroid regulatory system during fasting. |
| 2488 | 16210367 | Differential effects of central leptin, insulin, or glucose administration during fasting on the hypothalamic-pituitary-thyroid axis and feeding-related neurons in the arcuate nucleus. |
| 2489 | 16210367 | The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript. |
| 2490 | 16210367 | Because the central administration of leptin is capable of preventing the inhibitory effects of fasting on TRH mRNA in hypophysiotropic neurons primarily through effects on the arcuate nucleus, we determined whether the continuous administration of 30 mU/d insulin or 648 microg/d glucose into the cerebrospinal fluid by osmotic minipump might also have similar effects on the hypothalamic-pituitary-thyroid axis. |
| 2491 | 16210367 | As anticipated, the intracerebroventricular infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased proopiomelanocortin and cocaine and amphetamine-regulated transcript mRNA in the arcuate nucleus. |
| 2492 | 16210367 | In contrast, whereas insulin increased proopiomelanocortin mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA or circulating thyroid hormone levels. |
| 2493 | 16210367 | We conclude that insulin and glucose only partially replicate the central effects of leptin and may not be essential components of the hypothalamic-pituitary-thyroid regulatory system during fasting. |
| 2494 | 16250324 | Several research centers carried out collaborative studies of the nucleotide sequences of human and animal proopiomelanocortin (lipotropin precursor) and prolactin cDNA. |
| 2495 | 16250324 | Researchers constructed genetic engineering producers of human pre-proinsulin and somatostatin, identified structural genes expressed in pancreatic beta-cells, studied antigenic properties of glutamic acid decarboxylase (GAD), which determine insulin-dependent diabetes, and identified the cholesterase determinant. |
| 2496 | 16250324 | They revealed mutations in the genes of proopiomelanocortin and melanocortin receptors (MC4-P), which inhibit leptin regulation of appetite and are associated with human obesity. |
| 2497 | 16250324 | Several research centers carried out collaborative studies of the nucleotide sequences of human and animal proopiomelanocortin (lipotropin precursor) and prolactin cDNA. |
| 2498 | 16250324 | Researchers constructed genetic engineering producers of human pre-proinsulin and somatostatin, identified structural genes expressed in pancreatic beta-cells, studied antigenic properties of glutamic acid decarboxylase (GAD), which determine insulin-dependent diabetes, and identified the cholesterase determinant. |
| 2499 | 16250324 | They revealed mutations in the genes of proopiomelanocortin and melanocortin receptors (MC4-P), which inhibit leptin regulation of appetite and are associated with human obesity. |
| 2500 | 16284652 | We have generated mice that carry a neuron-specific leptin receptor (LEPR) transgene whose expression is driven by the rat synapsin I promoter synapsin-LEPR B (SYN-LEPR-B). |
| 2501 | 16284652 | We also show complete correction of the obesity and related phenotypes of db/db mice that are hemizygous for both NSE-LEPR-B and SYN-LEPR-B transgenes (Nse+Syn db/db). |
| 2502 | 16284652 | Body composition, insulin sensitivity, and cold tolerance were completely normalized in Nse+Syn db/db mice at 12 weeks of age compared with lean controls. |
| 2503 | 16284652 | In situ hybridization for LEPR B isoform expression in Nse+Syn db/db mice showed robust expression in the energy homeostasis-relevant regions of the hypothalamus. |
| 2504 | 16284652 | Expression of 3 neuropeptide genes, agouti-related peptide (Agrp), neuropeptide Y (Npy), and proopiomelanocortin (Pomc), was fully normalized in dual transgenic db/db mice. |
| 2505 | 16310285 | The melanocortin signaling system is orchestrated by two, independent groups of neurons in the hypothalamic arcuate nucleus with opposing functions that synthesize either alpha-melanocyte stimulating hormone (alpha-MSH) or agouti-related protein (AGRP). |
| 2506 | 16310285 | Alpha-MSH has an activating effect on hypophysiotropic TRH neurons via the phosphorylation of CREB, and when administered exogenously, can completely reverse fasting-induced suppression of TRH mRNA in the PVN. |
| 2507 | 16310285 | Inhibition of the HPT axis by fasting may be explained by inhibition of melanocortin signaling as a result of a reduction in alpha-MSH and increase in AGRP. |
| 2508 | 16310285 | Neuropeptide Y may also modulate the effects of the melanocortin signaling system during fasting by potentiating the inhibitory actions of AGRP on hypophysiotropic TRH neurons to prevent the phosphorylation of CREB and through direct inhibitory effects on alpha-MSH-producing neurons in the arcuate nucleus. |
| 2509 | 16310285 | The melanocortin signaling system is orchestrated by two, independent groups of neurons in the hypothalamic arcuate nucleus with opposing functions that synthesize either alpha-melanocyte stimulating hormone (alpha-MSH) or agouti-related protein (AGRP). |
| 2510 | 16310285 | Alpha-MSH has an activating effect on hypophysiotropic TRH neurons via the phosphorylation of CREB, and when administered exogenously, can completely reverse fasting-induced suppression of TRH mRNA in the PVN. |
| 2511 | 16310285 | Inhibition of the HPT axis by fasting may be explained by inhibition of melanocortin signaling as a result of a reduction in alpha-MSH and increase in AGRP. |
| 2512 | 16310285 | Neuropeptide Y may also modulate the effects of the melanocortin signaling system during fasting by potentiating the inhibitory actions of AGRP on hypophysiotropic TRH neurons to prevent the phosphorylation of CREB and through direct inhibitory effects on alpha-MSH-producing neurons in the arcuate nucleus. |
| 2513 | 16310285 | The melanocortin signaling system is orchestrated by two, independent groups of neurons in the hypothalamic arcuate nucleus with opposing functions that synthesize either alpha-melanocyte stimulating hormone (alpha-MSH) or agouti-related protein (AGRP). |
| 2514 | 16310285 | Alpha-MSH has an activating effect on hypophysiotropic TRH neurons via the phosphorylation of CREB, and when administered exogenously, can completely reverse fasting-induced suppression of TRH mRNA in the PVN. |
| 2515 | 16310285 | Inhibition of the HPT axis by fasting may be explained by inhibition of melanocortin signaling as a result of a reduction in alpha-MSH and increase in AGRP. |
| 2516 | 16310285 | Neuropeptide Y may also modulate the effects of the melanocortin signaling system during fasting by potentiating the inhibitory actions of AGRP on hypophysiotropic TRH neurons to prevent the phosphorylation of CREB and through direct inhibitory effects on alpha-MSH-producing neurons in the arcuate nucleus. |
| 2517 | 16310285 | The melanocortin signaling system is orchestrated by two, independent groups of neurons in the hypothalamic arcuate nucleus with opposing functions that synthesize either alpha-melanocyte stimulating hormone (alpha-MSH) or agouti-related protein (AGRP). |
| 2518 | 16310285 | Alpha-MSH has an activating effect on hypophysiotropic TRH neurons via the phosphorylation of CREB, and when administered exogenously, can completely reverse fasting-induced suppression of TRH mRNA in the PVN. |
| 2519 | 16310285 | Inhibition of the HPT axis by fasting may be explained by inhibition of melanocortin signaling as a result of a reduction in alpha-MSH and increase in AGRP. |
| 2520 | 16310285 | Neuropeptide Y may also modulate the effects of the melanocortin signaling system during fasting by potentiating the inhibitory actions of AGRP on hypophysiotropic TRH neurons to prevent the phosphorylation of CREB and through direct inhibitory effects on alpha-MSH-producing neurons in the arcuate nucleus. |
| 2521 | 16320160 | Alpha melanocyte-stimulating hormone (alpha-MSH) is an agonist at the melanocortin 3 (MC3-R) and melanocortin 4 (MC4-R) receptors. |
| 2522 | 16320160 | Agouti related protein (AgRP) is an endogenous antagonist at the MC3-R and MC4-R and is expressed in the rat adrenal cortex. |
| 2523 | 16320160 | AgRP antagonises alpha-MSH-induced corticosterone release from rat and bovine adrenal cells. |
| 2524 | 16320160 | Alpha melanocyte-stimulating hormone (alpha-MSH) is an agonist at the melanocortin 3 (MC3-R) and melanocortin 4 (MC4-R) receptors. |
| 2525 | 16320160 | Agouti related protein (AgRP) is an endogenous antagonist at the MC3-R and MC4-R and is expressed in the rat adrenal cortex. |
| 2526 | 16320160 | AgRP antagonises alpha-MSH-induced corticosterone release from rat and bovine adrenal cells. |
| 2527 | 16353609 | Studies in our laboratory and elsewhere have demonstrated numerous abnormalities of steroid and polypeptide hormone secretion in obesity: hyperestrogenemia and hypogonadotropic hypogonadism in obese men; diminished SHBG levels in both sexes; elevated free testosterone and free estradiol in obese women; PCOS-like gonadotropin and sex-hormone abnormalities in obese women; elevated serum insulin in both sexes; blunted stimulability of prolactin, growth hormone, and vasopressin in both sexes; and elevated basal levels and blunted stimulability and suppressibility of beta-endorphin in both sexes. |
| 2528 | 16390921 | Low estriol levels in the maternal triple-marker screen as a predictor of isolated adrenocorticotropic hormone deficiency caused by a new mutation in the TPIT gene. |
| 2529 | 16390921 | There are also occasional reports of prenatal diagnosis of IAD by findings on the maternal triple-marker screen (TMST), a combined serum analyte test that measures levels of alpha-fetoprotein, human chorionic gonadotropin, and unconjugated estriol for the detection of Down syndrome and open neural-tube defects. |
| 2530 | 16390921 | A low estriol level in the context of normal fetal sonography and growth, after exclusion of placental sulfatase deficiency and Smith-Lemli-Opitz syndrome, should raise the suspicion of deficient fetal steroidogenesis, which leads to decreased production of adrenal dehydroepiandrosterone sulfate. |
| 2531 | 16390921 | Normal levels of steroid sulfatase activity and 7-dehydrocholesterol ruled out X-linked ichthyosis and Smith-Lemli-Opitz syndrome, respectively. |
| 2532 | 16396514 | The ligand of primary interest for treatment of insulin resistance is alpha-melanocyte-stimulating hormone (alpha-MSH), which is derived, as are all melanocortins, from tissue-specific post-translational proteolytic processing of the pro-opiomelanocortin (POMC) precursor protein. |
| 2533 | 16396514 | Recent results have shown that alpha-MSH is the complement of leptin in the endocrine circuit, regulating bodyweight, food intake, and metabolic rate. alpha-MSH can decrease bodyweight, weight gain, and food intake in mice with diet-induced and genetic obesity. |
| 2534 | 16396514 | For instance, the POMC null mouse is extremely sensitive to insulin in an insulin tolerance test, while being otherwise euglycemic. |
| 2535 | 16396514 | The results from rodent studies with alpha-MSH suggest reciprocal effects: alpha-MSH appears to increase sensitivity to insulin when present in the CNS, while alpha-MSH in the periphery is necessary for insulin resistance. |
| 2536 | 16396514 | The ligand of primary interest for treatment of insulin resistance is alpha-melanocyte-stimulating hormone (alpha-MSH), which is derived, as are all melanocortins, from tissue-specific post-translational proteolytic processing of the pro-opiomelanocortin (POMC) precursor protein. |
| 2537 | 16396514 | Recent results have shown that alpha-MSH is the complement of leptin in the endocrine circuit, regulating bodyweight, food intake, and metabolic rate. alpha-MSH can decrease bodyweight, weight gain, and food intake in mice with diet-induced and genetic obesity. |
| 2538 | 16396514 | For instance, the POMC null mouse is extremely sensitive to insulin in an insulin tolerance test, while being otherwise euglycemic. |
| 2539 | 16396514 | The results from rodent studies with alpha-MSH suggest reciprocal effects: alpha-MSH appears to increase sensitivity to insulin when present in the CNS, while alpha-MSH in the periphery is necessary for insulin resistance. |
| 2540 | 16396514 | The ligand of primary interest for treatment of insulin resistance is alpha-melanocyte-stimulating hormone (alpha-MSH), which is derived, as are all melanocortins, from tissue-specific post-translational proteolytic processing of the pro-opiomelanocortin (POMC) precursor protein. |
| 2541 | 16396514 | Recent results have shown that alpha-MSH is the complement of leptin in the endocrine circuit, regulating bodyweight, food intake, and metabolic rate. alpha-MSH can decrease bodyweight, weight gain, and food intake in mice with diet-induced and genetic obesity. |
| 2542 | 16396514 | For instance, the POMC null mouse is extremely sensitive to insulin in an insulin tolerance test, while being otherwise euglycemic. |
| 2543 | 16396514 | The results from rodent studies with alpha-MSH suggest reciprocal effects: alpha-MSH appears to increase sensitivity to insulin when present in the CNS, while alpha-MSH in the periphery is necessary for insulin resistance. |
| 2544 | 16396514 | The ligand of primary interest for treatment of insulin resistance is alpha-melanocyte-stimulating hormone (alpha-MSH), which is derived, as are all melanocortins, from tissue-specific post-translational proteolytic processing of the pro-opiomelanocortin (POMC) precursor protein. |
| 2545 | 16396514 | Recent results have shown that alpha-MSH is the complement of leptin in the endocrine circuit, regulating bodyweight, food intake, and metabolic rate. alpha-MSH can decrease bodyweight, weight gain, and food intake in mice with diet-induced and genetic obesity. |
| 2546 | 16396514 | For instance, the POMC null mouse is extremely sensitive to insulin in an insulin tolerance test, while being otherwise euglycemic. |
| 2547 | 16396514 | The results from rodent studies with alpha-MSH suggest reciprocal effects: alpha-MSH appears to increase sensitivity to insulin when present in the CNS, while alpha-MSH in the periphery is necessary for insulin resistance. |
| 2548 | 16430857 | Brain serotonin (5-hydroxytryptamine; 5-HT) systems contribute to regulate eating behavior and energy homeostasis. 5-HT2C receptors and 5-HT1B receptors have been shown to mediate anorexic effects of 5-HT drugs such as d-fenfluramine, which stimulates 5-HT release and inhibits 5-HT reuptake, and m-chlorophenylpiperazine (mCPP), a 5-HT2C receptor agonist. |
| 2549 | 16430857 | Here, we report that 24-h fasting increased the expression of hypothalamic 5-HT2C receptor and 5-HT1B receptor genes in association with increases in plasma active ghrelin levels compared with fed state in mice. |
| 2550 | 16430857 | Treatment with mCPP or fenfluramine significantly inhibited the increases in plasma active ghrelin levels. mCPP or fenfluramine significantly increased the expression of hypothalamic pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript genes while having no significant effects on the expression of hypothalamic neuropeptide Y, agouti- related protein, and ghrelin genes. |
| 2551 | 16430857 | These results suggest that there is a negative feedback system between brain 5-HT systems and plasma active ghrelin levels in energy homeostasis in mice. |
| 2552 | 16437012 | Serum Growth hormone binding protein (GHBP), insulin growth factor I (IGF-I) and IGF binding protein (IGFBP) - 3 levels are all significantly decreased in patients with AN and return to normal with refeeding. |
| 2553 | 16437012 | IGFBP-1 and 2 are increased and return also to normal with weight gain. |
| 2554 | 16437012 | Corticotropin (ACTH) levels are normal with decreased response to Corticotropin releasing hormone (CRH). |
| 2555 | 16437012 | Finally leptin levels are decreased in patients with AN while ghrelin levels are elevated. |
| 2556 | 16437012 | Both leptin and ghrelin levels return to control values after renutrition. |
| 2557 | 16450289 | In conclusion, our results suggest that ginsenoside Rh2 may lower plasma glucose in STZ-diabetic rats based on an increase in beta-endorphin secretion that activates opioid mu-receptors thereby resulting in an increased expression of GLUT 4. |
| 2558 | 16475950 | In the hypothalamus, restorative gene therapy has been successfully implemented in Brattleboro rats, an arginine vasopressin (AVP) mutant which suffers from diabetes insipidus, in Koletsky (fa(k)/fa(k)) and in Zucker (fa/fa) rats which have leptin receptor mutations that render them obese, hyperphagic and hyperinsulinemic. |
| 2559 | 16475950 | In the above models, viral vectors expressing AVP, leptin receptor b and proopiomelanocortin, respectively were stereotaxically injected in the relevant hypothalamic regions. |
| 2560 | 16475950 | Stereotaxic injection of an adenoviral vector expressing Insulin-like Growth Factor-I (IGF-I) was able to correct their chronic hyperprolactinemia and restore tuberoinfundibular dopaminergic (TIDA) neuron numbers. |
| 2561 | 16480676 | Primary aldosteronism, congenital adrenal hyperplasia, Cushing's syndrome, glucocorticoid-remediable aldosteronism, and corticotropin-dependent forms of adrenal pathology can cause hypertension by excessive production of adrenocortical hormones. |
| 2562 | 16484325 | To investigate the role of ghrelin in the hyperphagia associated with uncontrolled streptozotocin-induced diabetes, food intake was followed in diabetic ghrelin knockout (ghrelin(-/-)) and control wild-type (ghrelin(+/+)) mice and diabetic Naval Medical Research Institute noninbred Swiss mice treated with either saline or the ghrelin receptor antagonist, D-Lys3-GH-releasing peptide-6 (D-Lys3-GHRP-6) for 5 d. |
| 2563 | 16484325 | In diabetic ghrelin(+/+) mice, but not in ghrelin(-/-) mice, the number of neuropeptide Y (NPY)-immunoreactive neurons was significantly increased. |
| 2564 | 16484325 | The change in the number of NPY- (2.4-fold increase) and alpha-MSH (1.7-fold decrease)-immunoreactive hypothalamic neurons induced by diabetes was normalized by D-Lys3-GHRP-6 treatment. |
| 2565 | 16484325 | Our results suggest that enhanced NPY and reduced alpha-MSH expression are secondary to the release of ghrelin, which should be considered the underlying trigger of hyperphagia associated with uncontrolled diabetes. |
| 2566 | 16484325 | To investigate the role of ghrelin in the hyperphagia associated with uncontrolled streptozotocin-induced diabetes, food intake was followed in diabetic ghrelin knockout (ghrelin(-/-)) and control wild-type (ghrelin(+/+)) mice and diabetic Naval Medical Research Institute noninbred Swiss mice treated with either saline or the ghrelin receptor antagonist, D-Lys3-GH-releasing peptide-6 (D-Lys3-GHRP-6) for 5 d. |
| 2567 | 16484325 | In diabetic ghrelin(+/+) mice, but not in ghrelin(-/-) mice, the number of neuropeptide Y (NPY)-immunoreactive neurons was significantly increased. |
| 2568 | 16484325 | The change in the number of NPY- (2.4-fold increase) and alpha-MSH (1.7-fold decrease)-immunoreactive hypothalamic neurons induced by diabetes was normalized by D-Lys3-GHRP-6 treatment. |
| 2569 | 16484325 | Our results suggest that enhanced NPY and reduced alpha-MSH expression are secondary to the release of ghrelin, which should be considered the underlying trigger of hyperphagia associated with uncontrolled diabetes. |
| 2570 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2571 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2572 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2573 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2574 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2575 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2576 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2577 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2578 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2579 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2580 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2581 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2582 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2583 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2584 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2585 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2586 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2587 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2588 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2589 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2590 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2591 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2592 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2593 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2594 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2595 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2596 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2597 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2598 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2599 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2600 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2601 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2602 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2603 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2604 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2605 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2606 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2607 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2608 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2609 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2610 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2611 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2612 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2613 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2614 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2615 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2616 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2617 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2618 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2619 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2620 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2621 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2622 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2623 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2624 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2625 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2626 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2627 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2628 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2629 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2630 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2631 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2632 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2633 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2634 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2635 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2636 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2637 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2638 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2639 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2640 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2641 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2642 | 16505217 | Divergent regulation of proopiomelanocortin neurons by leptin in the nucleus of the solitary tract and in the arcuate hypothalamic nucleus. |
| 2643 | 16505217 | Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin's central actions to influence energy balance. |
| 2644 | 16505217 | However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. |
| 2645 | 16505217 | The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. |
| 2646 | 16505217 | We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. |
| 2647 | 16505217 | In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. |
| 2648 | 16505217 | Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. |
| 2649 | 16505217 | We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. |
| 2650 | 16505217 | POMC neurons in the hypothalamus may therefore mediate all of leptin's signaling via POMC-derived peptides in the central nervous system. |
| 2651 | 16505249 | In conclusion, our results provide novel mechanisms for the plasma glucose-lowering action of metformin, via an increase of beta-endorphin secretion from adrenal glands to stimulate opioid mu-receptor linkage, leading to an increase of GLUT-4 gene expression and an attenuation of hepatic PEPCK gene expression in STZ-induced diabetic rats. |
| 2652 | 16523411 | Metformin increases insulin sensitivity and plasma beta-endorphin in human subjects. |
| 2653 | 16523411 | Fasting plasma glucose, A1C, HOMA-IR for insulin resistance, lipid profile, and plasma beta-endorphin-like immunoreactivity (BER) were measured before treatment and weekly at the end of each dosing period. |
| 2654 | 16523411 | In conclusion, metformin causes a significant parallel increase in insulin sensitivity and plasma beta-endorphin level in human subjects. |
| 2655 | 16523411 | Metformin increases insulin sensitivity and plasma beta-endorphin in human subjects. |
| 2656 | 16523411 | Fasting plasma glucose, A1C, HOMA-IR for insulin resistance, lipid profile, and plasma beta-endorphin-like immunoreactivity (BER) were measured before treatment and weekly at the end of each dosing period. |
| 2657 | 16523411 | In conclusion, metformin causes a significant parallel increase in insulin sensitivity and plasma beta-endorphin level in human subjects. |
| 2658 | 16523411 | Metformin increases insulin sensitivity and plasma beta-endorphin in human subjects. |
| 2659 | 16523411 | Fasting plasma glucose, A1C, HOMA-IR for insulin resistance, lipid profile, and plasma beta-endorphin-like immunoreactivity (BER) were measured before treatment and weekly at the end of each dosing period. |
| 2660 | 16523411 | In conclusion, metformin causes a significant parallel increase in insulin sensitivity and plasma beta-endorphin level in human subjects. |
| 2661 | 16611215 | The Melanocortin-4 Receptor is stimulated by endogenous melanocortin agonists derived from the pro-opiomelanocortin gene transcript and antagonized by the endogenous antagonist agouti-related protein. |
| 2662 | 16644867 | However, Pc1 knockout mice do not become obese; in fact, they are runted due to a defect in growth-hormone releasing hormone processing, leading to the speculation that PC1 subserves different functions between mouse and human. |
| 2663 | 16644867 | Here, we report a novel allele of mouse Pc1 (N222D) that leads to obesity, abnormal proinsulin processing and multiple endocrinological defects. |
| 2664 | 16644867 | The obesity is associated with impaired autocatalytic activation of mature PC1 and reduced hypothalamic alpha-MSH. |
| 2665 | 16721033 | The data support the assertion of a direct action of CRH on human adrenocortical cells in addition to an intra-adrenal CRH receptor/adrenocorticotropin system. |
| 2666 | 16794802 | Cushing's syndrome caused by adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is an extremely rare disease, which shows bilateral macronodular adrenal hypertrophy and autonomous cortisol production. |
| 2667 | 16809929 | In the hypothalamus, restorative gene therapy has been successfully implemented in Brattleboro rats, an arginine vasopressin (AVP) mutant which suffers from diabetes insipidus, and in Koletsky (fa(k)/fa(k)) and in Zucker (fa/fa) rats which have leptin receptor mutations that render them obese, hyperphagic and hyperinsulinemic. |
| 2668 | 16809929 | In the above models, viral vectors expressing AVP, leptin receptor b and proopiomelanocortin, respectively, were stereotaxically injected in the relevant hypothalamic regions. |
| 2669 | 16809929 | Stereotaxic injection of an adenoviral vector expressing insulin-like growth factor I corrected their chronic hyperprolactinemia and restored TIDA neuron numbers. |
| 2670 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 2671 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 2672 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 2673 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 2674 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 2675 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 2676 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 2677 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 2678 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 2679 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 2680 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 2681 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 2682 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 2683 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 2684 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 2685 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 2686 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 2687 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 2688 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 2689 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 2690 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 2691 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 2692 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 2693 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 2694 | 16825606 | Evidence that endogenous SST inhibits ACTH and ghrelin expression by independent pathways. |
| 2695 | 16825606 | Corticosterone and total ghrelin levels are increased in somatostatin (SST) knockout mice (Sst-/-) compared with SST-intact controls (Sst+/+). |
| 2696 | 16825606 | We report that Sst-/- mice had elevated mRNA levels for pituitary proopiomelanocortin (POMC), the precursor of adrenocorticotropic hormone (ACTH), whereas mRNA levels for hypothalamic corticotropin-releasing hormone (CRH) did not differ from Sst+/+ mice. |
| 2697 | 16825606 | Furthermore, SST suppressed pituitary POMC mRNA levels and ACTH release in vitro independently of CRH actions. |
| 2698 | 16825606 | In contrast, it has been reported that ghrelin increases glucocorticoids via a central effect on CRH secretion and that n-octanoyl ghrelin is the form of ghrelin that activates the GHS-R1a and modulates CRH neuronal activity. |
| 2699 | 16825606 | Because glucocorticoids and ghrelin increase in response to fasting, we examined the impact of fasting on the adrenal axis and ghrelin in Sst+/+ and Sst-/- mice and found that endogenous SST does not significantly contribute to this adaptive response. |
| 2700 | 16825606 | We conclude that endogenous SST inhibits basal ghrelin gene expression in a tissue specific manner and independently and directly inhibits pituitary ACTH synthesis and release. |
| 2701 | 16825606 | Thus endogenous SST exerts an inhibitory effect on ghrelin synthesis and on the adrenal axis through independent pathways. |
| 2702 | 16846990 | Immunohistochemical staining for follicle-stimulating hormone, luteinizing hormone, prolactin, human growth hormone, thyroid-stimulating hormone, and adrenocorticotropic hormone was applied to pituitary tissue from all cases. |
| 2703 | 16868891 | To address this issue, we determine the prevalence of neuroendocrine abnormalities in patients rehabilitating from severe traumatic brain injury (Glasgow Coma Scale < or = 8). 76 patients (mean age 39 +/- 14 yr; range 18-65; 53 males and 23 females; BMI 25.8 +/- 4.2 kg/m2; mean +/- SD) with a severe traumatic brain injury, an average of 22 +/- 10 months before this study (median, 20 months), underwent a series of standard endocrine tests, including TSH, free T4, T4, T3, prolactin, testosterone (males), estradiol (females), cortisol, ACTH, GH, and IGF-I. |
| 2704 | 16868891 | Pituitary deficiency was shown in 24% of the patients (18/76). 8% (n = 6) had GHD (GH-peak range [GHRH + arginine]: 2.8-6.3 microg/L; GH-peak range [ITT]: 1.5-2.2 microg/L; IGF-I range: 62-174 microg/L). 17% (n = 13) had hypogonadism (total testosterone < 9.5 nmol/L and low gonadotropins in 12 males; low estradiol, and low gonadotropins in 1 female). |
| 2705 | 16876574 | Adipose tissue secretes leptin, steroid hormones, adiponectin, inflammatory cytokines, resistin, complement factors, and vasoactive peptides. |
| 2706 | 16876574 | Leptin activates Janus-activating kinase2 (Jak2) and STAT 3, resulting in stimulation of anorexigenic peptides, e.g., alpha-MSH and CART, and inhibition of orexigenic peptides, e.g., NPY and AGRP. |
| 2707 | 16876574 | Leptin also stimulates fatty acid oxidation, insulin release, and peripheral insulin action. |
| 2708 | 16876574 | These effects involve regulation of PI-3 kinase, PTP-1B, suppressor of cytokine signaling-3 (SOCS-3), and AMP-activated protein kinase in the brain and peripheral organs. |
| 2709 | 16876574 | There is emerging evidence that leptin, adiponectin, and resistin act through overlapping pathways. |
| 2710 | 16876577 | Hypophysiotropic TRH neurons are located in the medial and periventricular parvocellular subdivisions of the PVN and receive direct monosynaptic projections from two, separate, populations of leptin-responsive neurons in the hypothalamic arcuate nucleus containing either alpha-melanocyte-stimulating hormone (alpha-MSH) and cocaine- and amphetamine-regulated transcript (CART), peptides that promote weight loss and increase energy expenditure, or neuropeptide Y (NPY) and agouti-related protein (AGRP), peptides that promote weight gain and reduce energy expenditure. |
| 2711 | 16876577 | During fasting, the reduction in TRH mRNA in hypophysiotropic neurons mediated by suppression of alpha-MSH/CART simultaneously with an increase in NPY/AGRP gene expression in arcuate nucleus neurons contributes to the fall in circulating thyroid hormone levels, presumably by increasing the sensitivity of the TRH gene to negative feedback inhibition by thyroid hormone. |
| 2712 | 16876577 | Endotoxin administration, however, has the paradoxical effect of increasing circulating levels of leptin and melanocortin signaling and CART gene expression in arcuate nucleus neurons, but inhibiting TRH gene expression in hypophysiotropic neurons. |
| 2713 | 16876577 | However, evidence that an anatomically separate population of nonhypophysiotropic TRH neurons in the anterior parvocellular subdivision of the PVN is integrated into the leptin regulatory control system by the same arcuate nucleus neuronal populations that innervate hypophysiotropic TRH neurons, raises the possibility that anterior parvocellular TRH neurons may be involved, possibly through interactions with the limbic nervous system. |
| 2714 | 16876577 | Hypophysiotropic TRH neurons are located in the medial and periventricular parvocellular subdivisions of the PVN and receive direct monosynaptic projections from two, separate, populations of leptin-responsive neurons in the hypothalamic arcuate nucleus containing either alpha-melanocyte-stimulating hormone (alpha-MSH) and cocaine- and amphetamine-regulated transcript (CART), peptides that promote weight loss and increase energy expenditure, or neuropeptide Y (NPY) and agouti-related protein (AGRP), peptides that promote weight gain and reduce energy expenditure. |
| 2715 | 16876577 | During fasting, the reduction in TRH mRNA in hypophysiotropic neurons mediated by suppression of alpha-MSH/CART simultaneously with an increase in NPY/AGRP gene expression in arcuate nucleus neurons contributes to the fall in circulating thyroid hormone levels, presumably by increasing the sensitivity of the TRH gene to negative feedback inhibition by thyroid hormone. |
| 2716 | 16876577 | Endotoxin administration, however, has the paradoxical effect of increasing circulating levels of leptin and melanocortin signaling and CART gene expression in arcuate nucleus neurons, but inhibiting TRH gene expression in hypophysiotropic neurons. |
| 2717 | 16876577 | However, evidence that an anatomically separate population of nonhypophysiotropic TRH neurons in the anterior parvocellular subdivision of the PVN is integrated into the leptin regulatory control system by the same arcuate nucleus neuronal populations that innervate hypophysiotropic TRH neurons, raises the possibility that anterior parvocellular TRH neurons may be involved, possibly through interactions with the limbic nervous system. |
| 2718 | 16926523 | Basal plasma levels of GH and insulin-like growth factor-I under fasting hyperglycemia (202 mg/dl) were markedly elevated. |
| 2719 | 16926523 | Plasma GH levels paradoxically increased after stimulation with TRH and LH-RH, and decreased after bromocriptine and octreotide administration. |
| 2720 | 16926523 | The tumor resected by transsphenoidal surgery was histopathologically consistent with the diagnosis of eosinophilic adenoma: positive immunoreactivities of GH, PRL and ACTH were demonstrated, but negative immunoreactivities of prohormone convertase (PC) 1/3 by immunohistochemical method. |
| 2721 | 16959056 | Fluvoxamine, a selective serotonin reuptake inhibitor, and 5-HT2C receptor inactivation induce appetite-suppressing effects in mice via 5-HT1B receptors. |
| 2722 | 16959056 | Moreover, CP 94253 (5-10 mg/kg), a selective 5-HT1B receptor agonist, exerted appetite-suppressing effects and significantly increased hypothalamic pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) gene expression and decreased hypothalamic orexin gene expression. |
| 2723 | 16959056 | These results suggest that fluvoxamine and inactivation of 5-HT2C receptors exert feeding suppression through activation of 5-HT1B receptors, and that 5-HT1B receptors up-regulate hypothalamic POMC and CART gene expression and down-regulate hypothalamic orexin gene expression in mice. |
| 2724 | 16959056 | Fluvoxamine, a selective serotonin reuptake inhibitor, and 5-HT2C receptor inactivation induce appetite-suppressing effects in mice via 5-HT1B receptors. |
| 2725 | 16959056 | Moreover, CP 94253 (5-10 mg/kg), a selective 5-HT1B receptor agonist, exerted appetite-suppressing effects and significantly increased hypothalamic pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) gene expression and decreased hypothalamic orexin gene expression. |
| 2726 | 16959056 | These results suggest that fluvoxamine and inactivation of 5-HT2C receptors exert feeding suppression through activation of 5-HT1B receptors, and that 5-HT1B receptors up-regulate hypothalamic POMC and CART gene expression and down-regulate hypothalamic orexin gene expression in mice. |
| 2727 | 16965293 | Young adult-specific hyperphagia in diabetic Goto-kakizaki rats is associated with leptin resistance and elevation of neuropeptide Y mRNA in the arcuate nucleus. |
| 2728 | 16965293 | In GK rats, leptin-induced phosphorylation of signal transducer and activator of transcription 3 was significantly reduced in the cells of the hypothalamic arcuate nucleus (ARC), but not of the ventromedial hypothalamus, whereas the mRNA level of functional leptin receptor was unaltered. |
| 2729 | 16965293 | By real-time polymerase chain reaction and in situ hybridisation, mRNA levels of neuropeptide Y, but not pro-opiomelanocortin and galanin-like peptide, were significantly increased in the ARC of GK rats at 11 weeks, but not 26 weeks. |
| 2730 | 16965293 | These results demonstrate that young adult GK rats display hyperphagia in association with leptin resistance and increased NPY mRNA level in the ARC. |
| 2731 | 17008116 | The cocaine and amphetamine regulated transcript (CART), an anorexigenic peptide responding to leptin, is expressed in various areas of the hypothalamus. |
| 2732 | 17008116 | Since CART plays an important role in the hypothalamic regulation of energy balance by reducing food intake and increasing lipid substrate utilization, it might affect cholesterol metabolism as Neuropeptide Y or pro-opiomelanocortin do. |
| 2733 | 17021375 | Leptin activates tyrosine kinase, Janus kinase 2, and signal transducer and activator of transcription 3, leading to increased levels of anorexigenic peptides, e.g., alpha-melanocyte stimulating hormone and cocaine- and amphetamine-regulated transcript, and inhibition of orexigenic peptides, e.g., neuropeptide Y and agouti-related peptide. |
| 2734 | 17021375 | Obesity is characterized by hyperleptinemia and hypothalamic leptin resistance, partly caused by induction of suppressor of cytokine signaling-3. |
| 2735 | 17021375 | Leptin also decreases glucose and stimulates lipolysis through central and peripheral pathways involving AMP-activated protein kinase (AMPK). |
| 2736 | 17021375 | Obesity, diabetes, and atherosclerosis have been associated with reduced adiponectin levels, whereas adiponectin treatment reverses these abnormalities partly through activation of AMPK in liver and muscle. |
| 2737 | 17021375 | Administration of adiponectin in the brain recapitulates the peripheral actions to increase fatty acid oxidation and insulin sensitivity and reduce glucose. |
| 2738 | 17021375 | As with leptin, adiponectin requires the central melanocortin pathway. |
| 2739 | 17021375 | Furthermore, adiponectin stimulates fatty acid oxidation and reduces glucose and lipids, at least in part, by activating AMPK in muscle and liver. |
| 2740 | 17023536 | Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding. |
| 2741 | 17023536 | Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). |
| 2742 | 17023536 | Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. |
| 2743 | 17023536 | To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. |
| 2744 | 17023536 | We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. |
| 2745 | 17023536 | These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response. |
| 2746 | 17023536 | Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding. |
| 2747 | 17023536 | Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). |
| 2748 | 17023536 | Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. |
| 2749 | 17023536 | To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. |
| 2750 | 17023536 | We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. |
| 2751 | 17023536 | These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response. |
| 2752 | 17023536 | Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding. |
| 2753 | 17023536 | Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). |
| 2754 | 17023536 | Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. |
| 2755 | 17023536 | To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. |
| 2756 | 17023536 | We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. |
| 2757 | 17023536 | These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response. |
| 2758 | 17023536 | Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding. |
| 2759 | 17023536 | Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). |
| 2760 | 17023536 | Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. |
| 2761 | 17023536 | To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. |
| 2762 | 17023536 | We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. |
| 2763 | 17023536 | These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response. |
| 2764 | 17023536 | Inactivation of signal transducer and activator of transcription 3 in proopiomelanocortin (Pomc) neurons causes decreased pomc expression, mild obesity, and defects in compensatory refeeding. |
| 2765 | 17023536 | Leptin is an adipocyte-derived hormone that signals body energy status to the brain by acting on multiple neuronal subgroups in the hypothalamus, including those that express proopiomelanocortin (Pomc) and agouti-related protein (Agrp). |
| 2766 | 17023536 | Signal transducer and activator of transcription 3 (Stat3) is an important intracellular signaling molecule activated by leptin, and previous studies have shown that mice carrying a mutated leptin receptor that abolished Stat3 binding are grossly obese. |
| 2767 | 17023536 | To determine the extent to which Stat3 signaling in Pomc neurons was responsible for these effects, we constructed Pomc-specific Stat3 mutants using a Cre recombinase transgene driven by the Pomc promoter. |
| 2768 | 17023536 | We find that Pomc expression is diminished in the mutant mice, suggesting that Stat3 is required for Pomc transcription. |
| 2769 | 17023536 | These results demonstrate a requirement for Stat3 in transcriptional regulation of Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response. |
| 2770 | 17032740 | Corticotropin-releasing factor and its receptors in the brain of rats with insulin and corticosterone deficits. |
| 2771 | 17032740 | The expression of genes encoding corticotropin-releasing factor (CRF) and its receptor type-1 (CRF1R) and type-2alpha (CRF2R) has been studied in the brain of rats with streptozotocin (STZ)-induced diabetes and adrenalectomy (ADX). |
| 2772 | 17032740 | STZ-diabetic rats demonstrated an induction of expression of CRF mRNA in the magnocellular part of the paraventricular hypothalamic nucleus (PVN) and in the supraoptic nucleus (SON), whereas the CRF transcript in the parvocellular PVN was significantly lower in rats with insulin deficiency. |
| 2773 | 17032740 | The present results suggest opposite effects of insulin and corticosterone deficiency on the hypophysiotropic CRF and the CRF1R mRNA contents, whereas the expression of CRF2R was mostly related to insulin, but not to the corticosterone status. |
| 2774 | 17032740 | Corticotropin-releasing factor and its receptors in the brain of rats with insulin and corticosterone deficits. |
| 2775 | 17032740 | The expression of genes encoding corticotropin-releasing factor (CRF) and its receptor type-1 (CRF1R) and type-2alpha (CRF2R) has been studied in the brain of rats with streptozotocin (STZ)-induced diabetes and adrenalectomy (ADX). |
| 2776 | 17032740 | STZ-diabetic rats demonstrated an induction of expression of CRF mRNA in the magnocellular part of the paraventricular hypothalamic nucleus (PVN) and in the supraoptic nucleus (SON), whereas the CRF transcript in the parvocellular PVN was significantly lower in rats with insulin deficiency. |
| 2777 | 17032740 | The present results suggest opposite effects of insulin and corticosterone deficiency on the hypophysiotropic CRF and the CRF1R mRNA contents, whereas the expression of CRF2R was mostly related to insulin, but not to the corticosterone status. |
| 2778 | 17039427 | Light microscopic and immunochemical studies revealed a pheochromocytoma that contained immunoreactive CRH and was negative for ACTH. |
| 2779 | 17050686 | Urocortin 2 modulates glucose utilization and insulin sensitivity in skeletal muscle. |
| 2780 | 17050686 | Urocortin 2 (Ucn 2), a member of the corticotropin-releasing factor (CRF) family, and its cognate type 2 CRF receptor (CRFR2) are highly expressed in skeletal muscle. |
| 2781 | 17050686 | In keeping with these data, Ucn 2 inhibited insulin-induced Akt and ERK1/2 phosphorylation in cultured skeletal muscle cells and C2C12 myotubes. |
| 2782 | 17050686 | These data are consistent with the hypothesis that Ucn 2 functions as a local negative regulator of glucose uptake in skeletal muscle and encourage exploration of the possibility that suppression of the Ucn 2/CRFR2 pathway may provide benefits in insulin-resistant states such as type 2 diabetes. |
| 2783 | 17072234 | Responses to ACTH or GHRH-arginine tests may be normal for several years though an ACTH and/or GH deficiency has been demonstrated by an insulin tolerance test, which is considered as the gold standard. |
| 2784 | 17082325 | In addition, we studied the effects of ACTH receptor (Mc2r) knockdown and dexamethasone (dex) on interrenal development and pituitary feedback. |
| 2785 | 17082325 | Until 2 d post fertilization (2 dpf) interrenal development assessed by transcripts of key steroidogenic genes (cyp11a1, mc2r, star) is independent of proopiomelanocortin (Pomc) as demonstrated in aal/eya1and lia/fgf3 mutants. |
| 2786 | 17082325 | In addition, we studied the effects of ACTH receptor (Mc2r) knockdown and dexamethasone (dex) on interrenal development and pituitary feedback. |
| 2787 | 17082325 | Until 2 d post fertilization (2 dpf) interrenal development assessed by transcripts of key steroidogenic genes (cyp11a1, mc2r, star) is independent of proopiomelanocortin (Pomc) as demonstrated in aal/eya1and lia/fgf3 mutants. |
| 2788 | 17097612 | Serotonin (5-hydroxytryptamine; 5-HT) 2A receptors contribute to the effects of 5-HT on platelet aggregation and vascular smooth muscle cell proliferation, and are reportedly involved in decreases in plasma levels of adiponectin, an adipokine, in diabetic subjects. |
| 2789 | 17097612 | Here, we report that systemic administration of sarpogrelate, a 5-HT2A receptor antagonist, suppressed appetite and increased hypothalamic pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript, corticotropin releasing hormone, 5-HT2C, and 5-HT1B receptor gene expression. |
| 2790 | 17097612 | These results suggest that obesity increases hypothalamic 5-HT2A receptor gene expression, and pharmacologic inactivation of 5-HT2A receptors inhibits overfeeding and obesity in A(y) mice, but did not increase plasma adiponectin levels. |
| 2791 | 17128564 | Mutations in the coding region of the ACTH receptor (MC2R) have been reported in several families with IGD. |
| 2792 | 17141181 | Akita male mice develop hyperphagia, reducing anorexigenic proopiomelanocortin (POMC), and increasing orexigenic neuropeptide Y (NPY) mRNA levels compared with wt males. |
| 2793 | 17141181 | While Akita female mice also developed hyperphagia, there was no difference in POMC, NPY and leptin levels between Akita and wt females. |
| 2794 | 17141181 | Anorexigenic Cocaine- and amphetamine-regulated transcript (CART) and corticotrophin-releasing factor (CRF) mRNA levels in Akita females were decreased against wt females. |
| 2795 | 17141181 | Akita male mice develop hyperphagia, reducing anorexigenic proopiomelanocortin (POMC), and increasing orexigenic neuropeptide Y (NPY) mRNA levels compared with wt males. |
| 2796 | 17141181 | While Akita female mice also developed hyperphagia, there was no difference in POMC, NPY and leptin levels between Akita and wt females. |
| 2797 | 17141181 | Anorexigenic Cocaine- and amphetamine-regulated transcript (CART) and corticotrophin-releasing factor (CRF) mRNA levels in Akita females were decreased against wt females. |
| 2798 | 17154037 | The hypophysitis presenting with central diabetes insipidus caused isolated adrenocorticotropic hormone (ACTH) deficiency after three years and two months since the onset of his illness. |
| 2799 | 17218412 | Haploinsufficiency in heterozygous glucokinase knockout mice produced effects similar to those produced by hypoglycemia: impaired reproductive function, elevated plasma corticosterone, increased food intake, and hypothalamic gene expression similar to that observed in fasted or leptin-deficient obese mice (increased hypothalamic neuropeptide Y mRNA and reduced hypothalamic proopiomelanocortin mRNA). |
| 2800 | 17218412 | Plasma glucose was elevated 2-fold in glucokinase knockout mice, consistent with a maturity-onset diabetes of the young phenotype, but plasma insulin and leptin levels were normal. |
| 2801 | 17218444 | Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. |
| 2802 | 17218444 | Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. |
| 2803 | 17218444 | Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. |
| 2804 | 17218444 | These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice. |
| 2805 | 17218444 | Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. |
| 2806 | 17218444 | Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. |
| 2807 | 17218444 | Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. |
| 2808 | 17218444 | These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice. |
| 2809 | 17218722 | Familial adrenocorticotropin-independent macronodular adrenal hyperplasia with aberrant serotonin and vasopressin adrenal receptors. |
| 2810 | 17250506 | Corticotropin and cortisol response to maximal exercise testing in central diabetes insipidus. |
| 2811 | 17261674 | Moreover, the mechanism involved in mediating glucose sensitivity in glucose-inhibited neurons and the neurotransmitter identity (neuropeptide Y [NPY] or pro-opio melanocortin [POMC]) of glucosensing neurons has remained controversial. |
| 2812 | 17261674 | Taken together, hypo- and hyperglycemia are detected by distinct populations of glucosensing neurons, and POMC and NPY neurons are not solely responsible for ARC glucosensing. |
| 2813 | 17261674 | Moreover, the mechanism involved in mediating glucose sensitivity in glucose-inhibited neurons and the neurotransmitter identity (neuropeptide Y [NPY] or pro-opio melanocortin [POMC]) of glucosensing neurons has remained controversial. |
| 2814 | 17261674 | Taken together, hypo- and hyperglycemia are detected by distinct populations of glucosensing neurons, and POMC and NPY neurons are not solely responsible for ARC glucosensing. |
| 2815 | 17283246 | CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor. |
| 2816 | 17283246 | Therefore, we analyzed CITED2, a CBP/p300 interacting transactivator with transforming activity, in the human adrenal gland. |
| 2817 | 17283246 | As ACTH and basic fibroblast growth factor (bFGF) are connected to the physiology and growth of adrenocortical cells we studied the regulation of CITED2 by these factors in the NCI-H295R adrenocortical carcinoma cell line. |
| 2818 | 17283246 | In NCI-H295R cells, stimulation by bFGF led to a dose-dependent increase in CITED2 promotor activity, mRNA and protein expression while ACTH had no significant effect. |
| 2819 | 17283246 | CITED2 is expressed in human adrenocortical cells and regulated by basic fibroblast growth factor. |
| 2820 | 17283246 | Therefore, we analyzed CITED2, a CBP/p300 interacting transactivator with transforming activity, in the human adrenal gland. |
| 2821 | 17283246 | As ACTH and basic fibroblast growth factor (bFGF) are connected to the physiology and growth of adrenocortical cells we studied the regulation of CITED2 by these factors in the NCI-H295R adrenocortical carcinoma cell line. |
| 2822 | 17283246 | In NCI-H295R cells, stimulation by bFGF led to a dose-dependent increase in CITED2 promotor activity, mRNA and protein expression while ACTH had no significant effect. |
| 2823 | 17286228 | Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. |
| 2824 | 17286228 | However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. |
| 2825 | 17286228 | Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. |
| 2826 | 17286228 | The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. |
| 2827 | 17286228 | This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach. |
| 2828 | 17286228 | Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. |
| 2829 | 17286228 | However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. |
| 2830 | 17286228 | Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. |
| 2831 | 17286228 | The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. |
| 2832 | 17286228 | This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach. |
| 2833 | 17286228 | Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. |
| 2834 | 17286228 | However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. |
| 2835 | 17286228 | Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. |
| 2836 | 17286228 | The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. |
| 2837 | 17286228 | This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach. |
| 2838 | 17286228 | Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. |
| 2839 | 17286228 | However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. |
| 2840 | 17286228 | Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. |
| 2841 | 17286228 | The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. |
| 2842 | 17286228 | This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach. |
| 2843 | 17286228 | Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. |
| 2844 | 17286228 | However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. |
| 2845 | 17286228 | Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. |
| 2846 | 17286228 | The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. |
| 2847 | 17286228 | This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach. |
| 2848 | 17334640 | RT-PCR analysis showed decreased proopiomelanocortin (POMC) mRNA expression and increased agouti-related protein (AGRP) mRNA expression in Ins2Akita mice. |
| 2849 | 17334640 | These observations indicate that Ins2Akita mice, which are characterized by hypoinsulinemia and hyperglycemia, exhibited hyperphagia and anxiety behavior; the mechanism of action involved the activation of hypothalamic AGRP and the inactivation of hypothalamic POMC. |
| 2850 | 17334640 | RT-PCR analysis showed decreased proopiomelanocortin (POMC) mRNA expression and increased agouti-related protein (AGRP) mRNA expression in Ins2Akita mice. |
| 2851 | 17334640 | These observations indicate that Ins2Akita mice, which are characterized by hypoinsulinemia and hyperglycemia, exhibited hyperphagia and anxiety behavior; the mechanism of action involved the activation of hypothalamic AGRP and the inactivation of hypothalamic POMC. |
| 2852 | 17360501 | Urocortin 3 regulates glucose-stimulated insulin secretion and energy homeostasis. |
| 2853 | 17360501 | Urocortin 3 (Ucn 3), a member of the corticotropin-releasing factor (CRF) family of peptides, is strongly expressed in mammalian pancreatic beta cells and has been shown to stimulate insulin secretion. |
| 2854 | 17360501 | Immunoneutralization of Ucn 3 or pharmacologic blockade of its receptor, the type 2 CRF receptor (CRFR2), attenuated high but not low glucose-induced insulin secretion from isolated islets in vitro. |
| 2855 | 17360501 | Consistently, peripheral injection of a selective CRFR2 antagonist before the administration of a glucose challenge significantly attenuated glucose-induced insulin secretion in vivo. |
| 2856 | 17397876 | Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. |
| 2857 | 17397876 | Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. |
| 2858 | 17397876 | Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. |
| 2859 | 17397876 | The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats. |
| 2860 | 17397876 | Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. |
| 2861 | 17397876 | Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. |
| 2862 | 17397876 | Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. |
| 2863 | 17397876 | The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats. |
| 2864 | 17397876 | Plasma glucose, insulin, beta-endorphin and adrenaline were assessed after intraperitoneal administration of serotonin. |
| 2865 | 17397876 | Serotonin produced hypoglycemic effects without altering plasma insulin and adrenaline levels but increasing beta-endorphin level in STZ-diabetic rats. |
| 2866 | 17397876 | Dihydroergotamine (non-selective 5-HT receptor blocker) and pimozide (5-HT(7) receptor blocker) abolished the hypoglycemic effect of serotonin in STZ-diabetic rats. |
| 2867 | 17397876 | The results demonstrated that serotonin may activate 5-HT(7) receptor on rat adrenal gland to enhance of beta-endorphin secretion, which then stimulates the opioid receptor to increase peripheral glucose utilization, resulting in decreased plasma glucose levels in STZ-diabetic rats. |
| 2868 | 17400800 | Real-time PCR was performed to characterise pro-opiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related protein (AgRP) and OBRb gene expression at the mRNA level. |
| 2869 | 17400800 | This phenotype also shows significant alterations in POMC, NPY, AgRP and OBRb gene expression together with elevations in circulating levels of both plasma leptin and insulin. |
| 2870 | 17400800 | Real-time PCR was performed to characterise pro-opiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related protein (AgRP) and OBRb gene expression at the mRNA level. |
| 2871 | 17400800 | This phenotype also shows significant alterations in POMC, NPY, AgRP and OBRb gene expression together with elevations in circulating levels of both plasma leptin and insulin. |
| 2872 | 17430247 | Although we have not yet identified the signal associated with sucrose drinking, the weight of mesenteric fat correlates inversely with hypothalamic corticotropin-releasing factor (CRF). |
| 2873 | 17430247 | When rats eat lard and sucrose ad libitum, fat stores increase and CRF, ACTH and corticosterone responses are reduced. |
| 2874 | 17430247 | Although we have not yet identified the signal associated with sucrose drinking, the weight of mesenteric fat correlates inversely with hypothalamic corticotropin-releasing factor (CRF). |
| 2875 | 17430247 | When rats eat lard and sucrose ad libitum, fat stores increase and CRF, ACTH and corticosterone responses are reduced. |
| 2876 | 17437948 | Among the neurotransmitters and neuropeptids of the hypothalamus, serotonin, norepinephrine, GABA, cholecystokinin, neuropeptide-Y, Agouti-related protein, alpha-MSH and ghrelin have essential importance in the eating disorders. |
| 2877 | 17437948 | The levels of leptin and galanin determine whether formation of anabolic or catabolic neurotransmitters should take place. |
| 2878 | 17439089 | At latest follow-up the following pituitary hormone deficiencies were identified: ACTH 19; TSH 20; testosterone 18; ADH (diabetes insipidus) eight. |
| 2879 | 17550779 | Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. |
| 2880 | 17550779 | To define the insulin-responsive neurons that mediate these effects, we generated mice with selective inactivation of the insulin receptor (IR) in either pro-opiomelanocortin (POMC)- or agouti-related peptide (AgRP)-expressing neurons of the arcuate nucleus of the hypothalamus. |
| 2881 | 17550779 | While neither POMC- nor AgRP-restricted IR knockout mice exhibited altered energy homeostasis, insulin failed to normally suppress hepatic glucose production during euglycemic-hyperinsulinemic clamps in AgRP-IR knockout (IR(DeltaAgRP)) mice. |
| 2882 | 17550779 | These mice also exhibited reduced insulin-stimulated hepatic interleukin-6 expression and increased hepatic expression of glucose-6-phosphatase. |
| 2883 | 17550779 | These results directly demonstrate that insulin action in POMC and AgRP cells is not required for steady-state regulation of food intake and body weight. |
| 2884 | 17550779 | However, insulin action specifically in AgRP-expressing neurons does play a critical role in controlling hepatic glucose production and may provide a target for the treatment of insulin resistance in type 2 diabetes. |
| 2885 | 17550779 | Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. |
| 2886 | 17550779 | To define the insulin-responsive neurons that mediate these effects, we generated mice with selective inactivation of the insulin receptor (IR) in either pro-opiomelanocortin (POMC)- or agouti-related peptide (AgRP)-expressing neurons of the arcuate nucleus of the hypothalamus. |
| 2887 | 17550779 | While neither POMC- nor AgRP-restricted IR knockout mice exhibited altered energy homeostasis, insulin failed to normally suppress hepatic glucose production during euglycemic-hyperinsulinemic clamps in AgRP-IR knockout (IR(DeltaAgRP)) mice. |
| 2888 | 17550779 | These mice also exhibited reduced insulin-stimulated hepatic interleukin-6 expression and increased hepatic expression of glucose-6-phosphatase. |
| 2889 | 17550779 | These results directly demonstrate that insulin action in POMC and AgRP cells is not required for steady-state regulation of food intake and body weight. |
| 2890 | 17550779 | However, insulin action specifically in AgRP-expressing neurons does play a critical role in controlling hepatic glucose production and may provide a target for the treatment of insulin resistance in type 2 diabetes. |
| 2891 | 17671657 | AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons. |
| 2892 | 17671657 | To directly address such issues, we generated POMC alpha 2KO and AgRP alpha 2KO mice lacking AMPK alpha2 in proopiomelanocortin- (POMC-) and agouti-related protein-expressing (AgRP-expressing) neurons, key regulators of energy homeostasis. |
| 2893 | 17671657 | Electrophysiological studies in AMPK alpha2-deficient POMC or AgRP neurons revealed normal leptin or insulin action but absent responses to alterations in extracellular glucose levels, showing that glucose-sensing signaling mechanisms in these neurons are distinct from those pathways utilized by leptin or insulin. |
| 2894 | 17671657 | Taken together with the divergent phenotypes of POMC alpha 2KO and AgRP alpha 2KO mice, our findings suggest that while AMPK plays a key role in hypothalamic function, it does not act as a general sensor and integrator of energy homeostasis in the mediobasal hypothalamus. |
| 2895 | 17671657 | AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons. |
| 2896 | 17671657 | To directly address such issues, we generated POMC alpha 2KO and AgRP alpha 2KO mice lacking AMPK alpha2 in proopiomelanocortin- (POMC-) and agouti-related protein-expressing (AgRP-expressing) neurons, key regulators of energy homeostasis. |
| 2897 | 17671657 | Electrophysiological studies in AMPK alpha2-deficient POMC or AgRP neurons revealed normal leptin or insulin action but absent responses to alterations in extracellular glucose levels, showing that glucose-sensing signaling mechanisms in these neurons are distinct from those pathways utilized by leptin or insulin. |
| 2898 | 17671657 | Taken together with the divergent phenotypes of POMC alpha 2KO and AgRP alpha 2KO mice, our findings suggest that while AMPK plays a key role in hypothalamic function, it does not act as a general sensor and integrator of energy homeostasis in the mediobasal hypothalamus. |
| 2899 | 17671657 | AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons. |
| 2900 | 17671657 | To directly address such issues, we generated POMC alpha 2KO and AgRP alpha 2KO mice lacking AMPK alpha2 in proopiomelanocortin- (POMC-) and agouti-related protein-expressing (AgRP-expressing) neurons, key regulators of energy homeostasis. |
| 2901 | 17671657 | Electrophysiological studies in AMPK alpha2-deficient POMC or AgRP neurons revealed normal leptin or insulin action but absent responses to alterations in extracellular glucose levels, showing that glucose-sensing signaling mechanisms in these neurons are distinct from those pathways utilized by leptin or insulin. |
| 2902 | 17671657 | Taken together with the divergent phenotypes of POMC alpha 2KO and AgRP alpha 2KO mice, our findings suggest that while AMPK plays a key role in hypothalamic function, it does not act as a general sensor and integrator of energy homeostasis in the mediobasal hypothalamus. |
| 2903 | 17671657 | AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons. |
| 2904 | 17671657 | To directly address such issues, we generated POMC alpha 2KO and AgRP alpha 2KO mice lacking AMPK alpha2 in proopiomelanocortin- (POMC-) and agouti-related protein-expressing (AgRP-expressing) neurons, key regulators of energy homeostasis. |
| 2905 | 17671657 | Electrophysiological studies in AMPK alpha2-deficient POMC or AgRP neurons revealed normal leptin or insulin action but absent responses to alterations in extracellular glucose levels, showing that glucose-sensing signaling mechanisms in these neurons are distinct from those pathways utilized by leptin or insulin. |
| 2906 | 17671657 | Taken together with the divergent phenotypes of POMC alpha 2KO and AgRP alpha 2KO mice, our findings suggest that while AMPK plays a key role in hypothalamic function, it does not act as a general sensor and integrator of energy homeostasis in the mediobasal hypothalamus. |
| 2907 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2908 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2909 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2910 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2911 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2912 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2913 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2914 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2915 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2916 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2917 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2918 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2919 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2920 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2921 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2922 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2923 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2924 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2925 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2926 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2927 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2928 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2929 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2930 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2931 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2932 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2933 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2934 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2935 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2936 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2937 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2938 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2939 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2940 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2941 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2942 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2943 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2944 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2945 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2946 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2947 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2948 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2949 | 17712724 | Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. |
| 2950 | 17712724 | Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. |
| 2951 | 17712724 | The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. |
| 2952 | 17712724 | ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. |
| 2953 | 17712724 | There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. |
| 2954 | 17712724 | The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. |
| 2955 | 17712724 | In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. |
| 2956 | 17724010 | He was euthyroid with positive thyroid antibodies, low cortisol, aldosterone and very high adrenocorticotropin (ActH) and renin levels. |
| 2957 | 17728716 | To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. |
| 2958 | 17728716 | The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. |
| 2959 | 17728716 | UCP2 negatively regulates glucose sensing in POMC neurons. |
| 2960 | 17728716 | To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. |
| 2961 | 17728716 | The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. |
| 2962 | 17728716 | UCP2 negatively regulates glucose sensing in POMC neurons. |
| 2963 | 17728716 | To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. |
| 2964 | 17728716 | The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. |
| 2965 | 17728716 | UCP2 negatively regulates glucose sensing in POMC neurons. |
| 2966 | 17853061 | DM type 2 is also accompanied by increased tissue levels of angiotensin II (Ang II), which stimulates the HPA axis through the Ang II type 1 receptors (AT1). |
| 2967 | 17853061 | In response to hCRH, time-integrated secretion of ACTH was not altered by candesartan administration, however, the cortisol response was decreased significantly compared to baseline (mean +/- SEM, 2327 +/- 148.3 vs. 1943 +/- 131.9 microg/dl, P = 0.005) suggesting reduced sensitivity of the adrenals to ACTH. |
| 2968 | 17884440 | We measured adrenal weight, plasma ACTH, serum and urinary corticosterone, and serum leptin in OLETF rats at 5 to 36 weeks of age. |
| 2969 | 17884440 | Overall, there was an inverse correlation between serum corticosterone and serum leptin (r = -0.374, P < .0005), whereas there was a positive correlation between plasma ACTH and serum leptin (r = 0.654, P < .0001). |
| 2970 | 17884440 | We measured adrenal weight, plasma ACTH, serum and urinary corticosterone, and serum leptin in OLETF rats at 5 to 36 weeks of age. |
| 2971 | 17884440 | Overall, there was an inverse correlation between serum corticosterone and serum leptin (r = -0.374, P < .0005), whereas there was a positive correlation between plasma ACTH and serum leptin (r = 0.654, P < .0001). |
| 2972 | 17943697 | A retrospective analysis of all histological and immunohistochemical slides rendered an adenoma exhibiting chromophobia, ACTH-positivity and features of atypia such as elevated p53 and Ki67 expression as well as nuclear polymorphism. |
| 2973 | 17992609 | In laboratory examination, plasma concentration of free thyroxine, thyroid stimulating hormone (TSH), cortisol, and adrenocorticotropic hormone (ACTH) was low. |
| 2974 | 17992609 | Provocative tests after delivery revealed a low response in TSH, prolactin (PRL), and follicle stimulating hormone (FSH). |
| 2975 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 2976 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 2977 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 2978 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 2979 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 2980 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 2981 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 2982 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 2983 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 2984 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 2985 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 2986 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 2987 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 2988 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 2989 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 2990 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 2991 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 2992 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 2993 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 2994 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 2995 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 2996 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 2997 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 2998 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 2999 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 3000 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 3001 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 3002 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 3003 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 3004 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 3005 | 18006626 | Maternal perinatal undernutrition drastically reduces postnatal leptin surge and affects the development of arcuate nucleus proopiomelanocortin neurons in neonatal male rat pups. |
| 3006 | 18006626 | The present study aimed at examining the impact of maternal undernutrition on leptin plasma levels in newborn male rats and on the arcuate nucleus proopiomelanocortin (POMC) and neuropeptide Y (NPY) neurons that are major leptin targets. |
| 3007 | 18006626 | Using a model of perinatal maternal 50% food-restricted diet (FR50) in the rat, we evaluated leptin plasma levels and hypothalamic POMC and NPY gene expression from postnatal day (PND) 4 to PND30 in both control and FR50 offspring. |
| 3008 | 18006626 | In FR50 animals, using semiquantitative RT-PCR and in situ hybridization, we showed that the hypothalamic POMC mRNA level was decreased from PND14 until PND30, whereas NPY gene expression was not significantly modified. |
| 3009 | 18006626 | In PND21 FR50 animals, we observed strikingly reduced immunoreactive beta-endorphin nerve fibers projecting to the hypothalamic paraventricular nucleus without affecting NPY projections. |
| 3010 | 18006626 | Our data showed that maternal undernutrition drastically reduces the postnatal surge of plasma leptin, disturbing particularly the hypothalamic wiring as well as the gene expression of the anorexigenic POMC neurons in male rat pups. |
| 3011 | 18018629 | [Case of small cell lung cancer complicated with diabetes insipidus and Cushing syndrome due to ectopic adrenocorticotropic hormone secretion]. |
| 3012 | 18018629 | We concluded that this case was Cushing syndrome caused by ectopic adrenocorticotropic hormone-producing small cell lung cancer, and that it presented with diabetes insipidus because of pituitary metastasis. |
| 3013 | 18018629 | [Case of small cell lung cancer complicated with diabetes insipidus and Cushing syndrome due to ectopic adrenocorticotropic hormone secretion]. |
| 3014 | 18018629 | We concluded that this case was Cushing syndrome caused by ectopic adrenocorticotropic hormone-producing small cell lung cancer, and that it presented with diabetes insipidus because of pituitary metastasis. |
| 3015 | 18058602 | Conversely, corticotrophin-releasing hormone (CRH) and melanotan-II (MT-II, a synthetic structural homologue of alpha-melanocyte-stimulating hormone, alphaMSH) inhibit feeding behavior. |
| 3016 | 18058602 | After bilateral electrolytic lesions of the PVN, rats were given ghrelin intraperitoneally (i. p.), or intracerebroventricular (i. c. v.) infusion of CRH or MT-II. |
| 3017 | 18058602 | We measured the cumulative food intake (FI) for 4 h after ghrelin injection in rats fed AD LIB, and the changes in FI at 15 min, 30 min, 1 h, and 2 h after infusion of CRH and MT-II in rats fasted for 24 h. |
| 3018 | 18058602 | Thus, ghrelin and CRH showed more potent orexigenic and anorectic effects in PVN-lesioned rats, respectively, but MT-II lost its inhibitory action on feeding behavior. |
| 3019 | 18058602 | These results suggest that the hyperphagia and obesity induced by PVN lesions may be related to an increased orexigenic action of ghrelin due to the destruction of endogenous CRH and alphaMSH receptors. |
| 3020 | 18128849 | Results of the study suggest, therefore, that ACTH may prove to be as effective in the control of chronic non-Addisonian hypoglycemosis as insulin is in the control of diabetes mellitus. |
| 3021 | 18183075 | In the present study, to investigate the effect of hyperglycemia on the function of 5-HT2A receptors, we compared the 5-HT2A receptor-mediated wet-dog shake responses in rats treated with adrenocorticotropic hormone (ACTH), dexamethasone and streptozotocin. |
| 3022 | 18183075 | The wet-dog shake responses induced by (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a 5-HT2A receptor agonist, were significantly enhanced at 14 days after repeated treatment with ACTH and dexamethasone. |
| 3023 | 18183075 | In the present study, to investigate the effect of hyperglycemia on the function of 5-HT2A receptors, we compared the 5-HT2A receptor-mediated wet-dog shake responses in rats treated with adrenocorticotropic hormone (ACTH), dexamethasone and streptozotocin. |
| 3024 | 18183075 | The wet-dog shake responses induced by (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a 5-HT2A receptor agonist, were significantly enhanced at 14 days after repeated treatment with ACTH and dexamethasone. |
| 3025 | 18209867 | The gestation dramatically affects the maternal hypothalamic-pituitary-adrenal axis, resulting in increased hepatic production of corticosteroid-binding globulin (CBG), increased levels of serum, salivary and urinary free cortisol, lack of suppression of cortisol levels after dexamethasone administration and placental production of CRH and ACTH. |
| 3026 | 18270844 | Thyroid-stimulating hormone (TSH) and ACTH deficiency occur after intensive irradiation only (>50 Gy) with a long-term cumulative frequency of 3-6%. |
| 3027 | 18338267 | A minimum set of pre-operative endocrine tests should include serum electrolytes, cortisol (at 08.00-09.00 h), free-T4, TSH, prolactin, oestradiol/testosterone, LH, FSH and IGF-1. |
| 3028 | 18338267 | Some clinicians will choose to perform pre-operative Synacthen or insulin tolerance testing to further define ACTH reserve. |
| 3029 | 18421906 | The various hormones, proteins and other compounds related to developing obesity, insulin resistance and type 2 diabetes are analyzed in the paper. 1) Leptin, ciliary neurutrophic factor, adiponectin, glucagon-like peptide 1, peptide YY, neuromedin S, as well as the protein receptors of these hormones decrease the food consumption, increase the energy turnover, and prevent obesity, insulin resistance, and type 2 diabetes development. |
| 3030 | 18421906 | The mediators of these hormone and receptor actions are melanocyte stimulating hormone (MSH), corticotropin-releasing hormone (CRH), and the others. 2) Ghrelin, endogenose cannabinoides, galanin-like peptide and the mediators of their actions: neuropeptide Y (NPY) and Agouti gene related protein (AGRP) increase the appetite and food consumption. |
| 3031 | 18439911 | Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin. |
| 3032 | 18439911 | We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females. |
| 3033 | 18439911 | RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression. |
| 3034 | 18439911 | These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene. |
| 3035 | 18439911 | Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin. |
| 3036 | 18439911 | We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females. |
| 3037 | 18439911 | RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression. |
| 3038 | 18439911 | These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene. |
| 3039 | 18439911 | Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin. |
| 3040 | 18439911 | We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females. |
| 3041 | 18439911 | RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression. |
| 3042 | 18439911 | These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene. |
| 3043 | 18439911 | Ablation of estrogen receptor alpha (ERalpha) prevents upregulation of POMC by leptin and insulin. |
| 3044 | 18439911 | We investigated the role of estrogen receptor alpha (ERalpha) in the regulation of the hypothalamic POMC in females. |
| 3045 | 18439911 | RT-PCR showed a significant attenuation of POMC expression in both ERaKOAkt and ERaKO mice, irrespective of the elevated leptin serum levels or hyperinsulinemia, while elevated serum leptin levels in AFO and B6FO mice upregulated POMC gene expression. |
| 3046 | 18439911 | These results indicate that ERalpha plays an essential role in leptin- and insulin-stimulated upregulation of the POMC gene. |
| 3047 | 18477467 | Serotonin systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors and induce anorexia via a leptin-independent pathway in mice. |
| 3048 | 18477467 | NEFA/nucleobindin2 (NUCB2), a novel satiety molecule, is associated with leptin-independent melanocortin signaling in the central nervous system. |
| 3049 | 18477467 | Here, we show that systemic administration of m-chlorophenylpiperazine (mCPP), a serotonin 5-HT1B/2C receptor agonist, significantly increased the expression of hypothalamic NUCB2 in wild-type mice. |
| 3050 | 18477467 | The increases in hypothalamic NUCB2 expression induced by mCPP were attenuated in 5-HT2C receptor mutant mice. |
| 3051 | 18477467 | On the other hand, the expression of hypothalamic NUCB2 and proopiomelanocortin (POMC) was significantly decreased in hyperphagic and non-obese 5-HT2C receptor mutants compared with age-matched wild-type mice. |
| 3052 | 18477467 | Interestingly, despite increased expression of hypothalamic POMC, hypothalamic NUCB2 expression was decreased in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene. |
| 3053 | 18477467 | These findings suggest that 5-HT systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors, and induce anorexia via a leptin-independent pathway in mice. |
| 3054 | 18477467 | Serotonin systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors and induce anorexia via a leptin-independent pathway in mice. |
| 3055 | 18477467 | NEFA/nucleobindin2 (NUCB2), a novel satiety molecule, is associated with leptin-independent melanocortin signaling in the central nervous system. |
| 3056 | 18477467 | Here, we show that systemic administration of m-chlorophenylpiperazine (mCPP), a serotonin 5-HT1B/2C receptor agonist, significantly increased the expression of hypothalamic NUCB2 in wild-type mice. |
| 3057 | 18477467 | The increases in hypothalamic NUCB2 expression induced by mCPP were attenuated in 5-HT2C receptor mutant mice. |
| 3058 | 18477467 | On the other hand, the expression of hypothalamic NUCB2 and proopiomelanocortin (POMC) was significantly decreased in hyperphagic and non-obese 5-HT2C receptor mutants compared with age-matched wild-type mice. |
| 3059 | 18477467 | Interestingly, despite increased expression of hypothalamic POMC, hypothalamic NUCB2 expression was decreased in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene. |
| 3060 | 18477467 | These findings suggest that 5-HT systems upregulate the expression of hypothalamic NUCB2 via 5-HT2C receptors, and induce anorexia via a leptin-independent pathway in mice. |
| 3061 | 18551113 | The aim of this study was to investigate a series of single-nucleotide polymorphisms (SNPs) in the genes MC2R, MC3R, MC4R, MC5R, POMC, and ENPP1 for association with obesity. |
| 3062 | 18551113 | Weaker associations were detected between the SNPs rs1541276 in the MC5R, rs1926065 in the MC3R genes and obesity (P = 0.04 and P = 0.03, respectively), and between SNPs rs2236700 in the MC5R, rs2118404 in the POMC, rs943003 in the ENPP1 genes and type 2 diabetes (P = 0.03, P = 0.02 and P = 0.02, respectively); these associations did not, however, remain significant after correction for multiple testing. |
| 3063 | 18551113 | In this study, we did not find association between the frequently studied ENPP1 K121Q variant, nor SNPs in the MCR or POMC genes and obesity or type 2 diabetes. |
| 3064 | 18551113 | The aim of this study was to investigate a series of single-nucleotide polymorphisms (SNPs) in the genes MC2R, MC3R, MC4R, MC5R, POMC, and ENPP1 for association with obesity. |
| 3065 | 18551113 | Weaker associations were detected between the SNPs rs1541276 in the MC5R, rs1926065 in the MC3R genes and obesity (P = 0.04 and P = 0.03, respectively), and between SNPs rs2236700 in the MC5R, rs2118404 in the POMC, rs943003 in the ENPP1 genes and type 2 diabetes (P = 0.03, P = 0.02 and P = 0.02, respectively); these associations did not, however, remain significant after correction for multiple testing. |
| 3066 | 18551113 | In this study, we did not find association between the frequently studied ENPP1 K121Q variant, nor SNPs in the MCR or POMC genes and obesity or type 2 diabetes. |
| 3067 | 18551113 | The aim of this study was to investigate a series of single-nucleotide polymorphisms (SNPs) in the genes MC2R, MC3R, MC4R, MC5R, POMC, and ENPP1 for association with obesity. |
| 3068 | 18551113 | Weaker associations were detected between the SNPs rs1541276 in the MC5R, rs1926065 in the MC3R genes and obesity (P = 0.04 and P = 0.03, respectively), and between SNPs rs2236700 in the MC5R, rs2118404 in the POMC, rs943003 in the ENPP1 genes and type 2 diabetes (P = 0.03, P = 0.02 and P = 0.02, respectively); these associations did not, however, remain significant after correction for multiple testing. |
| 3069 | 18551113 | In this study, we did not find association between the frequently studied ENPP1 K121Q variant, nor SNPs in the MCR or POMC genes and obesity or type 2 diabetes. |
| 3070 | 18551122 | The objectives of this study were to identify potential alterations in gene expression of melanocortin-4 receptor (MC4-R), proopiomelanocortin (POMC), and Agouti-related protein (AgRP) in mouse hypothalamus under a chronic peripheral infusion of leptin or at early (8 weeks) and advanced (16 weeks) phases of diet-induced obesity. |
| 3071 | 18551122 | We reported that in control mice, but not in obese mice, leptin infusion induced an increase in POMC mRNA level as well as in MC4-R mRNA level suggesting that leptin could act directly and/or through alpha-melanocyte-stimulating hormone (alpha-MSH). |
| 3072 | 18551122 | This hypothesis was reinforced after in vitro studies, using the mouse hypothalamic GT1-7 cell line, since both leptin and Norleucine(4), D-Phenylalanine(7)-alpha-MSH (NDP-alpha-MSH) treatments increased MC4-R expression. |
| 3073 | 18551122 | After 8 weeks of high-fat diet, nondiabetic obese mice became resistant to the central action of leptin and their hypothalamic content of POMC and AgRP mRNA were decreased without modification of MC4-R mRNA level. |
| 3074 | 18551122 | The objectives of this study were to identify potential alterations in gene expression of melanocortin-4 receptor (MC4-R), proopiomelanocortin (POMC), and Agouti-related protein (AgRP) in mouse hypothalamus under a chronic peripheral infusion of leptin or at early (8 weeks) and advanced (16 weeks) phases of diet-induced obesity. |
| 3075 | 18551122 | We reported that in control mice, but not in obese mice, leptin infusion induced an increase in POMC mRNA level as well as in MC4-R mRNA level suggesting that leptin could act directly and/or through alpha-melanocyte-stimulating hormone (alpha-MSH). |
| 3076 | 18551122 | This hypothesis was reinforced after in vitro studies, using the mouse hypothalamic GT1-7 cell line, since both leptin and Norleucine(4), D-Phenylalanine(7)-alpha-MSH (NDP-alpha-MSH) treatments increased MC4-R expression. |
| 3077 | 18551122 | After 8 weeks of high-fat diet, nondiabetic obese mice became resistant to the central action of leptin and their hypothalamic content of POMC and AgRP mRNA were decreased without modification of MC4-R mRNA level. |
| 3078 | 18551122 | The objectives of this study were to identify potential alterations in gene expression of melanocortin-4 receptor (MC4-R), proopiomelanocortin (POMC), and Agouti-related protein (AgRP) in mouse hypothalamus under a chronic peripheral infusion of leptin or at early (8 weeks) and advanced (16 weeks) phases of diet-induced obesity. |
| 3079 | 18551122 | We reported that in control mice, but not in obese mice, leptin infusion induced an increase in POMC mRNA level as well as in MC4-R mRNA level suggesting that leptin could act directly and/or through alpha-melanocyte-stimulating hormone (alpha-MSH). |
| 3080 | 18551122 | This hypothesis was reinforced after in vitro studies, using the mouse hypothalamic GT1-7 cell line, since both leptin and Norleucine(4), D-Phenylalanine(7)-alpha-MSH (NDP-alpha-MSH) treatments increased MC4-R expression. |
| 3081 | 18551122 | After 8 weeks of high-fat diet, nondiabetic obese mice became resistant to the central action of leptin and their hypothalamic content of POMC and AgRP mRNA were decreased without modification of MC4-R mRNA level. |
| 3082 | 18551122 | The objectives of this study were to identify potential alterations in gene expression of melanocortin-4 receptor (MC4-R), proopiomelanocortin (POMC), and Agouti-related protein (AgRP) in mouse hypothalamus under a chronic peripheral infusion of leptin or at early (8 weeks) and advanced (16 weeks) phases of diet-induced obesity. |
| 3083 | 18551122 | We reported that in control mice, but not in obese mice, leptin infusion induced an increase in POMC mRNA level as well as in MC4-R mRNA level suggesting that leptin could act directly and/or through alpha-melanocyte-stimulating hormone (alpha-MSH). |
| 3084 | 18551122 | This hypothesis was reinforced after in vitro studies, using the mouse hypothalamic GT1-7 cell line, since both leptin and Norleucine(4), D-Phenylalanine(7)-alpha-MSH (NDP-alpha-MSH) treatments increased MC4-R expression. |
| 3085 | 18551122 | After 8 weeks of high-fat diet, nondiabetic obese mice became resistant to the central action of leptin and their hypothalamic content of POMC and AgRP mRNA were decreased without modification of MC4-R mRNA level. |
| 3086 | 18551299 | The subtotally resected lesion consisted of synaptophysin-immunoreactive lobules of (a) large, polygonal, amphophilic, PAS-positive cells immunoreactive for ACTH, beta-endorphin, alpha melanocyte stimulating hormone (MSH), and keratin (CAM5.2) in some cells showing Crooke hyaline change, (b) less frequent acidophilic, growth hormone (GH) immunoreactive cells, and (c) rare luteinizing hormone (LH) and/or alpha subunit immunopositive cells. |
| 3087 | 18551299 | Also conspicuous were smaller cells resembling Rathke-type epithelium forming rosettes to sizable glands immunoreactive for EMA, keratin, S-100 protein, galectin-3 and rarely for synaptophysin and/or one of the above-noted adenohypophysial hormones. |
| 3088 | 18551299 | Transcription factors, including Neuro-D1 and Pit-1, were present in ACTH- and GH-producing cells, respectively, but only in occasional Rathke-type cells. |
| 3089 | 18551299 | The subtotally resected lesion consisted of synaptophysin-immunoreactive lobules of (a) large, polygonal, amphophilic, PAS-positive cells immunoreactive for ACTH, beta-endorphin, alpha melanocyte stimulating hormone (MSH), and keratin (CAM5.2) in some cells showing Crooke hyaline change, (b) less frequent acidophilic, growth hormone (GH) immunoreactive cells, and (c) rare luteinizing hormone (LH) and/or alpha subunit immunopositive cells. |
| 3090 | 18551299 | Also conspicuous were smaller cells resembling Rathke-type epithelium forming rosettes to sizable glands immunoreactive for EMA, keratin, S-100 protein, galectin-3 and rarely for synaptophysin and/or one of the above-noted adenohypophysial hormones. |
| 3091 | 18551299 | Transcription factors, including Neuro-D1 and Pit-1, were present in ACTH- and GH-producing cells, respectively, but only in occasional Rathke-type cells. |
| 3092 | 18753263 | Among the neuropeptides analyzed [including oxytocin, vasopressin, thyrotropin-releasing hormone, and corticotropin-releasing factor (CRF)], FosB was only identified in CRF-positive neurons. |
| 3093 | 18971258 | At the termination of the experiment, hypothalamic mRNA expression levels of neuropeptide Y (NPY), agouti-related protein (AGRP), proopiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), orexin, brain-derived neurotropic factor (BDNF), phosphatase with tensin homology (Pten), melanocortin-3 receptor (MC3R), and NPY-Y1R were determined. |
| 3094 | 18971258 | Gene expression profiles identified exercise as having a significant effect on hypothalamic POMC, orexin, and MC3R levels. |
| 3095 | 18971258 | Genotype had a significant effect on AGRP, POMC, CART, and NPY-Y1R, with an exercise and genotype interaction effect on NPY gene expression. |
| 3096 | 18971258 | At the termination of the experiment, hypothalamic mRNA expression levels of neuropeptide Y (NPY), agouti-related protein (AGRP), proopiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), orexin, brain-derived neurotropic factor (BDNF), phosphatase with tensin homology (Pten), melanocortin-3 receptor (MC3R), and NPY-Y1R were determined. |
| 3097 | 18971258 | Gene expression profiles identified exercise as having a significant effect on hypothalamic POMC, orexin, and MC3R levels. |
| 3098 | 18971258 | Genotype had a significant effect on AGRP, POMC, CART, and NPY-Y1R, with an exercise and genotype interaction effect on NPY gene expression. |
| 3099 | 18971258 | At the termination of the experiment, hypothalamic mRNA expression levels of neuropeptide Y (NPY), agouti-related protein (AGRP), proopiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), orexin, brain-derived neurotropic factor (BDNF), phosphatase with tensin homology (Pten), melanocortin-3 receptor (MC3R), and NPY-Y1R were determined. |
| 3100 | 18971258 | Gene expression profiles identified exercise as having a significant effect on hypothalamic POMC, orexin, and MC3R levels. |
| 3101 | 18971258 | Genotype had a significant effect on AGRP, POMC, CART, and NPY-Y1R, with an exercise and genotype interaction effect on NPY gene expression. |
| 3102 | 19026699 | Based on the reported anti-inflammatory and anti-stress responses by corticotropin-releasing factor (CRF) receptor signaling, endogenous CRF receptor agonists, CRF, urocortin (UCN) I and its related peptides, may play protective roles against cardiovascular stresses via the CRF receptor signaling. |
| 3103 | 19026699 | In addition, due to the possible involvement of CRF receptor signaling in the effects of statin on endothelial cells, the effects of pitavastatin on the expression of UCN-related peptides in HAECs were also evaluated. |
| 3104 | 19026699 | HAECs expressed all UCNs, CRF type 1 receptor (CRF-R1), and CRF type 2 (CRF-R2)alpha and CRF-R2beta mRNAs. |
| 3105 | 19026699 | Real time PCR analysis revealed that UCN I mRNA was down-regulated, whereas UCN II mRNA was up-regulated by tumor necrosis factor (TNF)-alpha. |
| 3106 | 19026699 | Selective blockade of CRF-R1 resulted in significant increase in TNF-alpha-induced expression of vascular adhesion molecule-1 at mRNA level and E-selectin at mRNA and protein levels. |
| 3107 | 19026699 | On the contrary, UCN II, CRF-R1, and CRF-R2 mRNAs were markedly increased by co-incubation of pitavastatin and TNF-alpha. |
| 3108 | 19026699 | These facts indicate that CRF-R1 signaling may have protective role against TNF-alpha-induced vascular inflammation. |
| 3109 | 19026699 | In addition, because of up-regulation of CRF-R1 mRNA by pitavastatin with or without TNF-alpha, CRF-R1 may be involved in the vasoprotective effects of pitavastatin. |
| 3110 | 19039818 | We can conclude that cerebrocrast may regulate food intake and body weight through glucose sensing by proopiomelanocortin (POMC) neurons, that are involved in control of glucose homeostasis, stimulation of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion, activation of MC4-Rs and inhibition of neuropeptide Y (NPY) in the ARC of the hypothalamus, affecting the kidney, and causing decreased urine output and water intake. |
| 3111 | 19059526 | Because of the possible relationship between alpha-MSH and obesity, we endeavored to test the hypothesis that higher levels of alpha-MSH in obese patients would correlate with leptin levels and with other markers of obesity. |
| 3112 | 19059526 | Weight, measures of body composition, and diet diaries were obtained; fasting blood was analyzed for alpha-MSH, lipids, glucose, insulin, leptin, and adiponectin. |
| 3113 | 19059526 | Measures of adiposity correlated with insulin and leptin in men and women, and with adiponectin in women. alpha-Melanocyte-stimulating hormone levels did not correlate significantly with any parameter of adiposity or diet composition. |
| 3114 | 19059526 | Because of the possible relationship between alpha-MSH and obesity, we endeavored to test the hypothesis that higher levels of alpha-MSH in obese patients would correlate with leptin levels and with other markers of obesity. |
| 3115 | 19059526 | Weight, measures of body composition, and diet diaries were obtained; fasting blood was analyzed for alpha-MSH, lipids, glucose, insulin, leptin, and adiponectin. |
| 3116 | 19059526 | Measures of adiposity correlated with insulin and leptin in men and women, and with adiponectin in women. alpha-Melanocyte-stimulating hormone levels did not correlate significantly with any parameter of adiposity or diet composition. |
| 3117 | 19059526 | Because of the possible relationship between alpha-MSH and obesity, we endeavored to test the hypothesis that higher levels of alpha-MSH in obese patients would correlate with leptin levels and with other markers of obesity. |
| 3118 | 19059526 | Weight, measures of body composition, and diet diaries were obtained; fasting blood was analyzed for alpha-MSH, lipids, glucose, insulin, leptin, and adiponectin. |
| 3119 | 19059526 | Measures of adiposity correlated with insulin and leptin in men and women, and with adiponectin in women. alpha-Melanocyte-stimulating hormone levels did not correlate significantly with any parameter of adiposity or diet composition. |
| 3120 | 19150989 | Here, we show that BBS proteins are required for leptin receptor (LepR) signaling in the hypothalamus. |
| 3121 | 19150989 | We found that Bbs2(-/-), Bbs4(-/-) and Bbs6(-/-) mice are resistant to the action of leptin to reduce body weight and food intake regardless of serum leptin levels and obesity. |
| 3122 | 19150989 | In addition, activation of hypothalamic STAT3 by leptin is significantly decreased in Bbs2(-/-), Bbs4(-/-) and Bbs6(-/-) mice. |
| 3123 | 19150989 | In contrast, downstream melanocortin receptor signaling is unaffected, indicating that LepR signaling is specifically impaired in Bbs2(-/-), Bbs4(-/-) and Bbs6(-/-) mice. |
| 3124 | 19150989 | Impaired LepR signaling in BBS mice was associated with decreased Pomc gene expression. |
| 3125 | 19150989 | Furthermore, we found that BBS1 protein physically interacts with the LepR and that loss of BBS proteins perturbs LepR trafficking. |
| 3126 | 19150989 | Our data indicate that BBS proteins mediate LepR trafficking and that impaired LepR signaling underlies energy imbalance in BBS. |
| 3127 | 19279289 | In contrast, plasma leptin was only increased by insulin and diet, plasma glucagon and liver glycogen was only affected by insulin and liver triglycerides, and arcuate nucleus proopiomelanocortin mRNA was only influenced by diet. |
| 3128 | 19337797 | Association between variants in the genes for leptin, leptin receptor, and proopiomelanocortin with chronic heart failure in the Czech population. |
| 3129 | 19337797 | The aim of this study was to investigate the possible associations of defined variability in leptin (dbSNP ID rs7799039), proopiomelanocortin (dbSNP ID rs3754860 and dbSNP ID rs1009388), and leptin receptor gene (dbSNP rs1137101) with CHF and evaluate their potential as the CHF susceptibility genes. |
| 3130 | 19337797 | They were genotyped for the leptin (LEP) -2548 G/A, leptin receptor (LEPR) Gln223Arg, and proopiomelanocortin (POMC) RsaI (5'-untranslated region) and C1032G variants (intron 1) using PCR-based methodology. |
| 3131 | 19337797 | Association between variants in the genes for leptin, leptin receptor, and proopiomelanocortin with chronic heart failure in the Czech population. |
| 3132 | 19337797 | The aim of this study was to investigate the possible associations of defined variability in leptin (dbSNP ID rs7799039), proopiomelanocortin (dbSNP ID rs3754860 and dbSNP ID rs1009388), and leptin receptor gene (dbSNP rs1137101) with CHF and evaluate their potential as the CHF susceptibility genes. |
| 3133 | 19337797 | They were genotyped for the leptin (LEP) -2548 G/A, leptin receptor (LEPR) Gln223Arg, and proopiomelanocortin (POMC) RsaI (5'-untranslated region) and C1032G variants (intron 1) using PCR-based methodology. |
| 3134 | 19337797 | Association between variants in the genes for leptin, leptin receptor, and proopiomelanocortin with chronic heart failure in the Czech population. |
| 3135 | 19337797 | The aim of this study was to investigate the possible associations of defined variability in leptin (dbSNP ID rs7799039), proopiomelanocortin (dbSNP ID rs3754860 and dbSNP ID rs1009388), and leptin receptor gene (dbSNP rs1137101) with CHF and evaluate their potential as the CHF susceptibility genes. |
| 3136 | 19337797 | They were genotyped for the leptin (LEP) -2548 G/A, leptin receptor (LEPR) Gln223Arg, and proopiomelanocortin (POMC) RsaI (5'-untranslated region) and C1032G variants (intron 1) using PCR-based methodology. |
| 3137 | 19362483 | The complications included permanent diabetes insipidus, hypocortisolism (including a patient with a coexisting adrenocorticotropic hormone-secreting adenoma), sinusitis and a case of meningitis and intrasellar abscess, one year post-surgery. |
| 3138 | 19390493 | Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats. |
| 3139 | 19390493 | Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor, results in severe obesity, hyperglycaemia, and hyperinsulinemia. |
| 3140 | 19390493 | Our aim was to investigate the expression of STAT3 and its downstream effector proopiomelanocortin (POMC) in IUGR rats obtained by uterine artery ligation. |
| 3141 | 19390493 | At birth, hypothalamus was dissected and processed to evaluate the expression of STAT3, its phosphorylated form, and POMC. |
| 3142 | 19390493 | STAT3 mRNA, STAT3 protein, phosphorylated STAT3, POMC mRNA, and POMC protein were significantly reduced in IUGR versus sham animals (p < 0.0001, p < 0.05 and p < 0.001, p < 0.01, p < 0.01, respectively). |
| 3143 | 19390493 | Our results suggest that an abnormal intrauterine milieu can affect the hypothalamic expression of STAT3 and POMC at birth, altering the hypothalamic signaling pathways that regulate the energy homeostasis. |
| 3144 | 19390493 | Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats. |
| 3145 | 19390493 | Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor, results in severe obesity, hyperglycaemia, and hyperinsulinemia. |
| 3146 | 19390493 | Our aim was to investigate the expression of STAT3 and its downstream effector proopiomelanocortin (POMC) in IUGR rats obtained by uterine artery ligation. |
| 3147 | 19390493 | At birth, hypothalamus was dissected and processed to evaluate the expression of STAT3, its phosphorylated form, and POMC. |
| 3148 | 19390493 | STAT3 mRNA, STAT3 protein, phosphorylated STAT3, POMC mRNA, and POMC protein were significantly reduced in IUGR versus sham animals (p < 0.0001, p < 0.05 and p < 0.001, p < 0.01, p < 0.01, respectively). |
| 3149 | 19390493 | Our results suggest that an abnormal intrauterine milieu can affect the hypothalamic expression of STAT3 and POMC at birth, altering the hypothalamic signaling pathways that regulate the energy homeostasis. |
| 3150 | 19390493 | Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats. |
| 3151 | 19390493 | Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor, results in severe obesity, hyperglycaemia, and hyperinsulinemia. |
| 3152 | 19390493 | Our aim was to investigate the expression of STAT3 and its downstream effector proopiomelanocortin (POMC) in IUGR rats obtained by uterine artery ligation. |
| 3153 | 19390493 | At birth, hypothalamus was dissected and processed to evaluate the expression of STAT3, its phosphorylated form, and POMC. |
| 3154 | 19390493 | STAT3 mRNA, STAT3 protein, phosphorylated STAT3, POMC mRNA, and POMC protein were significantly reduced in IUGR versus sham animals (p < 0.0001, p < 0.05 and p < 0.001, p < 0.01, p < 0.01, respectively). |
| 3155 | 19390493 | Our results suggest that an abnormal intrauterine milieu can affect the hypothalamic expression of STAT3 and POMC at birth, altering the hypothalamic signaling pathways that regulate the energy homeostasis. |
| 3156 | 19390493 | Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats. |
| 3157 | 19390493 | Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor, results in severe obesity, hyperglycaemia, and hyperinsulinemia. |
| 3158 | 19390493 | Our aim was to investigate the expression of STAT3 and its downstream effector proopiomelanocortin (POMC) in IUGR rats obtained by uterine artery ligation. |
| 3159 | 19390493 | At birth, hypothalamus was dissected and processed to evaluate the expression of STAT3, its phosphorylated form, and POMC. |
| 3160 | 19390493 | STAT3 mRNA, STAT3 protein, phosphorylated STAT3, POMC mRNA, and POMC protein were significantly reduced in IUGR versus sham animals (p < 0.0001, p < 0.05 and p < 0.001, p < 0.01, p < 0.01, respectively). |
| 3161 | 19390493 | Our results suggest that an abnormal intrauterine milieu can affect the hypothalamic expression of STAT3 and POMC at birth, altering the hypothalamic signaling pathways that regulate the energy homeostasis. |
| 3162 | 19390493 | Exposure to uteroplacental insufficiency reduces the expression of signal transducer and activator of transcription 3 and proopiomelanocortin in the hypothalamus of newborn rats. |
| 3163 | 19390493 | Disruption of the signal transducer and activator of transcription 3 (STAT3) in the hypothalamic neurons expressing leptin receptor, results in severe obesity, hyperglycaemia, and hyperinsulinemia. |
| 3164 | 19390493 | Our aim was to investigate the expression of STAT3 and its downstream effector proopiomelanocortin (POMC) in IUGR rats obtained by uterine artery ligation. |
| 3165 | 19390493 | At birth, hypothalamus was dissected and processed to evaluate the expression of STAT3, its phosphorylated form, and POMC. |
| 3166 | 19390493 | STAT3 mRNA, STAT3 protein, phosphorylated STAT3, POMC mRNA, and POMC protein were significantly reduced in IUGR versus sham animals (p < 0.0001, p < 0.05 and p < 0.001, p < 0.01, p < 0.01, respectively). |
| 3167 | 19390493 | Our results suggest that an abnormal intrauterine milieu can affect the hypothalamic expression of STAT3 and POMC at birth, altering the hypothalamic signaling pathways that regulate the energy homeostasis. |
| 3168 | 19429177 | The obtained results suggest that the improvement of insulin sensitivity by agmatine is produced by two mechanisms, stimulation of adrenal gland to enhance beta-endorphin secretion and a direct activation of peripheral I2-imidazoline receptor in tissues, for the amelioration of insulin action. |
| 3169 | 19449282 | LPS significantly increased the serum levels of TNF-alpha and IL-6 in normal and diabetic rats; LPS also dramatically increased the plasma concentrations of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone. |
| 3170 | 19449282 | Both 0.1 and 1 mg/kg MLT doses significantly decreased the serum levels of TNF-alpha and IL-6. |
| 3171 | 19449282 | Significant inhibitory effects of MLT (1 mg/kg) were observed on the plasma concentrations of CRH, ACTH, and corticosterone of the HPA axis. |
| 3172 | 19449282 | LPS significantly increased the serum levels of TNF-alpha and IL-6 in normal and diabetic rats; LPS also dramatically increased the plasma concentrations of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone. |
| 3173 | 19449282 | Both 0.1 and 1 mg/kg MLT doses significantly decreased the serum levels of TNF-alpha and IL-6. |
| 3174 | 19449282 | Significant inhibitory effects of MLT (1 mg/kg) were observed on the plasma concentrations of CRH, ACTH, and corticosterone of the HPA axis. |
| 3175 | 19525593 | Neither adrenocorticotropic hormone (ACTH) nor cortisol levels were adequately increased in response to a mixed intravenous administration of corticotropin-releasing hormone, growth hormone-releasing hormone, thyrotropin-releasing hormone and lutenizing hormone-releasing hormone, although other pituitary hormones were increased adequately. |
| 3176 | 19565027 | Defects in this steroidogenic enzyme, the product of the CYP21A2 gene, cause disruption in the pathway involved in cortisol and aldosterone production and consequently, the accumulation of their steroid precursors as well as a resulting adrenocorticotrophic hormone (ACTH)-driven overproduction of adrenal androgens. |
| 3177 | 19636197 | Adrenocorticotropin-independent Cushing's syndrome in pregnancy related to overexpression of adrenal luteinizing hormone/human chorionic gonadotropin receptors. |
| 3178 | 19697135 | There were 93 nonfunctioning adenomas, 58 growth hormone-secreting, 41 prolactin-secreting, 28 adrenocorticotropin hormone secreting, 7 FSH-LH secreting and 1 thyroid-stimulating hormone-secreting adenomas. |
| 3179 | 19697135 | The remission results for patients with nonfunctioning adenomas was 83% and for functioning adenomas were 76.3% (70.6% for GH hormone-secreting, 85.3% for prolactin hormone-secreting, 71.4% for ACTH hormone-secreting, 85.7% for FSH-LH hormone-secreting and 100% for TSH hormone-secreting), with no recurrence at the time of the last follow-up. |
| 3180 | 19697135 | There were 93 nonfunctioning adenomas, 58 growth hormone-secreting, 41 prolactin-secreting, 28 adrenocorticotropin hormone secreting, 7 FSH-LH secreting and 1 thyroid-stimulating hormone-secreting adenomas. |
| 3181 | 19697135 | The remission results for patients with nonfunctioning adenomas was 83% and for functioning adenomas were 76.3% (70.6% for GH hormone-secreting, 85.3% for prolactin hormone-secreting, 71.4% for ACTH hormone-secreting, 85.7% for FSH-LH hormone-secreting and 100% for TSH hormone-secreting), with no recurrence at the time of the last follow-up. |
| 3182 | 19767734 | The obesity susceptibility gene Cpe links FoxO1 signaling in hypothalamic pro-opiomelanocortin neurons with regulation of food intake. |
| 3183 | 19767734 | Insulin and leptin inhibit food intake through actions in the central nervous system that are partly mediated by the transcription factor FoxO1. |
| 3184 | 19767734 | We show that FoxO1 ablation in pro-opiomelanocortin (Pomc)-expressing neurons in mice (here called Pomc-Foxo1(-/-) mice) increases Carboxypeptidase E (Cpe) expression, resulting in selective increases of alpha-melanocyte-stimulating hormone (alpha-Msh) and carboxy-cleaved beta-endorphin, the products of Cpe-dependent processing of Pomc. |
| 3185 | 19767734 | We show that Cpe expression is downregulated by diet-induced obesity and that FoxO1 deletion offsets the decrease, protecting against weight gain. |
| 3186 | 19767734 | Moreover, moderate Cpe overexpression in the arcuate nucleus phenocopies features of the FoxO1 mutation. |
| 3187 | 19767734 | The obesity susceptibility gene Cpe links FoxO1 signaling in hypothalamic pro-opiomelanocortin neurons with regulation of food intake. |
| 3188 | 19767734 | Insulin and leptin inhibit food intake through actions in the central nervous system that are partly mediated by the transcription factor FoxO1. |
| 3189 | 19767734 | We show that FoxO1 ablation in pro-opiomelanocortin (Pomc)-expressing neurons in mice (here called Pomc-Foxo1(-/-) mice) increases Carboxypeptidase E (Cpe) expression, resulting in selective increases of alpha-melanocyte-stimulating hormone (alpha-Msh) and carboxy-cleaved beta-endorphin, the products of Cpe-dependent processing of Pomc. |
| 3190 | 19767734 | We show that Cpe expression is downregulated by diet-induced obesity and that FoxO1 deletion offsets the decrease, protecting against weight gain. |
| 3191 | 19767734 | Moreover, moderate Cpe overexpression in the arcuate nucleus phenocopies features of the FoxO1 mutation. |
| 3192 | 19768550 | Inferior petrosal sinus ACTH and prolactin responses to CRH in ACTH-dependent Cushing's syndrome: a single centre experience from the United Kingdom. |
| 3193 | 19768550 | The maximal central/peripheral prolactin ratio was noted at 5 min post-CRH, coinciding with the maximal central/peripheral ACTH ratio. |
| 3194 | 19768550 | The intersinus gradient (ISG) of ACTH was paralleled by a consistent ISG of prolactin and in 7 out of 9 patients (with successful bilateral IPSS and unilateral adenomas) the ISG of prolactin correctly lateralized the microadenoma whereas the ISG of ACTH correctly lateralized in 8 out of 9 patients. |
| 3195 | 19768550 | Prolactin measurements do not have superior lateralizing capability compared with ACTH but may be useful in the differential diagnosis of pituitary-driven from EAS. |
| 3196 | 19768550 | Inferior petrosal sinus ACTH and prolactin responses to CRH in ACTH-dependent Cushing's syndrome: a single centre experience from the United Kingdom. |
| 3197 | 19768550 | The maximal central/peripheral prolactin ratio was noted at 5 min post-CRH, coinciding with the maximal central/peripheral ACTH ratio. |
| 3198 | 19768550 | The intersinus gradient (ISG) of ACTH was paralleled by a consistent ISG of prolactin and in 7 out of 9 patients (with successful bilateral IPSS and unilateral adenomas) the ISG of prolactin correctly lateralized the microadenoma whereas the ISG of ACTH correctly lateralized in 8 out of 9 patients. |
| 3199 | 19768550 | Prolactin measurements do not have superior lateralizing capability compared with ACTH but may be useful in the differential diagnosis of pituitary-driven from EAS. |
| 3200 | 19768550 | Inferior petrosal sinus ACTH and prolactin responses to CRH in ACTH-dependent Cushing's syndrome: a single centre experience from the United Kingdom. |
| 3201 | 19768550 | The maximal central/peripheral prolactin ratio was noted at 5 min post-CRH, coinciding with the maximal central/peripheral ACTH ratio. |
| 3202 | 19768550 | The intersinus gradient (ISG) of ACTH was paralleled by a consistent ISG of prolactin and in 7 out of 9 patients (with successful bilateral IPSS and unilateral adenomas) the ISG of prolactin correctly lateralized the microadenoma whereas the ISG of ACTH correctly lateralized in 8 out of 9 patients. |
| 3203 | 19768550 | Prolactin measurements do not have superior lateralizing capability compared with ACTH but may be useful in the differential diagnosis of pituitary-driven from EAS. |
| 3204 | 19768550 | Inferior petrosal sinus ACTH and prolactin responses to CRH in ACTH-dependent Cushing's syndrome: a single centre experience from the United Kingdom. |
| 3205 | 19768550 | The maximal central/peripheral prolactin ratio was noted at 5 min post-CRH, coinciding with the maximal central/peripheral ACTH ratio. |
| 3206 | 19768550 | The intersinus gradient (ISG) of ACTH was paralleled by a consistent ISG of prolactin and in 7 out of 9 patients (with successful bilateral IPSS and unilateral adenomas) the ISG of prolactin correctly lateralized the microadenoma whereas the ISG of ACTH correctly lateralized in 8 out of 9 patients. |
| 3207 | 19768550 | Prolactin measurements do not have superior lateralizing capability compared with ACTH but may be useful in the differential diagnosis of pituitary-driven from EAS. |
| 3208 | 19813002 | Accordingly, the patient was diagnosed as having ACTH-independent macronodular adrenal hyperplasia (AIMAH) with subclinical Cushing's syndrome associated with the aberrant expression of β-adrenergic receptors. |
| 3209 | 19882253 | Hormonal evaluation included 8.00 a.m. cortisol, DHEA-S, ACTH and in hypertensive subjects, plasma renin activity, and serum aldosterone. |
| 3210 | 19907099 | Ghrelin has a stimulating effect on arginine vasopressin (AVP). |
| 3211 | 19907099 | However, it is not known whether GHRP-2, a synthetic ghrelin receptor agonist, also has a stimulating effect on AVP release in men. |
| 3212 | 19907099 | There were no significant differences in hematocrit, blood pressure and plasma osmolality before and after GFRP-2 injection, although significant (p<0.001) peak blood GH, and ACTH and PRL levels were observed 30 and 15 min after GHRP-2 injection with and without fasting, respectively, and the maximal peaks were significantly (p<0.05) higher with fasting than without fasting. |
| 3213 | 19907099 | These results suggest that AVP secretion is not stimulated by the GHRP-2 test both with and without fasting, though GH, ACTH and PRL levels were higher with than without fasting. |
| 3214 | 19907099 | Ghrelin has a stimulating effect on arginine vasopressin (AVP). |
| 3215 | 19907099 | However, it is not known whether GHRP-2, a synthetic ghrelin receptor agonist, also has a stimulating effect on AVP release in men. |
| 3216 | 19907099 | There were no significant differences in hematocrit, blood pressure and plasma osmolality before and after GFRP-2 injection, although significant (p<0.001) peak blood GH, and ACTH and PRL levels were observed 30 and 15 min after GHRP-2 injection with and without fasting, respectively, and the maximal peaks were significantly (p<0.05) higher with fasting than without fasting. |
| 3217 | 19907099 | These results suggest that AVP secretion is not stimulated by the GHRP-2 test both with and without fasting, though GH, ACTH and PRL levels were higher with than without fasting. |
| 3218 | 19933072 | Laboratory work-up revealed panhypopituitarism (central diabetes insipidus; hypothyroidism; and low prolactin, gonadotrophin, and adrenocorticotropic hormone levels), and magnetic resonance imaging confirmed the pituitary and hypothalamic involvement. |
| 3219 | 19933998 | Divergent regulation of energy expenditure and hepatic glucose production by insulin receptor in agouti-related protein and POMC neurons. |
| 3220 | 19945028 | Pituitary abscess is a rare but potentially life-threatening disease and, in 30-50% of patients, anterior pituitary hormone deficiencies or central diabetes insipidus (DI) at onset may be observed: the earliest manifestation being growth hormone deficiency (GHD), followed by follicle-stimulating hormone (FSH)/luteinising hormone (LH), thyroid-stimulating hormone (TSH) and ACTH deficiencies. |
| 3221 | 19955787 | Candidate gene variants for polygenic obesity appear to disrupt pathways involved in the regulation of energy intake and expenditure and include adrenergic receptors, uncoupling proteins, PPARG, POMC, MC4R and a set of single nucleotide polymorphisms in the FTO locus. |
| 3222 | 20011966 | Mutations related to human monogenic obesity have been described in leptin, leptin receptor, proopiomelanocortin, prohormone convertase 1 or melanocortin receptor 4 genes. |
| 3223 | 20032567 | Histological examinations by needle biopsy of liver tumors in S5 and S8 indicated metastatic ACTH-producing NET, which was also confirmed by venous sampling. |
| 3224 | 20176722 | Third-trimester fetuses from mothers on HFD showed increases in proopiomelanocortin mRNA expression, whereas agouti-related protein mRNA and peptide levels were decreased in comparison with CTR fetuses. |
| 3225 | 20186151 | Moreover, the expression of corticotropin (MC2R) and angiotensin II type 1 (AT1R) receptors and 17alpha-hydroxylase in the tumors of these two patients was analyzed by immunohistochemistry. |
| 3226 | 20186151 | In both cases, immunostaining showed weak expression of AT1R and MC2R but strong expression of 17alpha-hydroxylase. |
| 3227 | 20374961 | Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. |
| 3228 | 20374961 | Circulating leptin and insulin convey information regarding energy stores to the central nervous system, particularly the hypothalamus. |
| 3229 | 20374961 | Hypothalamic pro-opiomelanocortin (POMC) neurons regulate energy balance and glucose homeostasis and express leptin and insulin receptors. |
| 3230 | 20374961 | However, the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established. |
| 3231 | 20374961 | Here, we show that mice lacking both leptin and insulin receptors in POMC neurons (Pomc-Cre, Lepr(flox/flox) IR(flox/flox) mice) display systemic insulin resistance, which is distinct from the single deletion of either receptor. |
| 3232 | 20374961 | We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function. |
| 3233 | 20374961 | Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. |
| 3234 | 20374961 | Circulating leptin and insulin convey information regarding energy stores to the central nervous system, particularly the hypothalamus. |
| 3235 | 20374961 | Hypothalamic pro-opiomelanocortin (POMC) neurons regulate energy balance and glucose homeostasis and express leptin and insulin receptors. |
| 3236 | 20374961 | However, the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established. |
| 3237 | 20374961 | Here, we show that mice lacking both leptin and insulin receptors in POMC neurons (Pomc-Cre, Lepr(flox/flox) IR(flox/flox) mice) display systemic insulin resistance, which is distinct from the single deletion of either receptor. |
| 3238 | 20374961 | We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function. |
| 3239 | 20374961 | Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. |
| 3240 | 20374961 | Circulating leptin and insulin convey information regarding energy stores to the central nervous system, particularly the hypothalamus. |
| 3241 | 20374961 | Hypothalamic pro-opiomelanocortin (POMC) neurons regulate energy balance and glucose homeostasis and express leptin and insulin receptors. |
| 3242 | 20374961 | However, the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established. |
| 3243 | 20374961 | Here, we show that mice lacking both leptin and insulin receptors in POMC neurons (Pomc-Cre, Lepr(flox/flox) IR(flox/flox) mice) display systemic insulin resistance, which is distinct from the single deletion of either receptor. |
| 3244 | 20374961 | We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function. |
| 3245 | 20374961 | Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. |
| 3246 | 20374961 | Circulating leptin and insulin convey information regarding energy stores to the central nervous system, particularly the hypothalamus. |
| 3247 | 20374961 | Hypothalamic pro-opiomelanocortin (POMC) neurons regulate energy balance and glucose homeostasis and express leptin and insulin receptors. |
| 3248 | 20374961 | However, the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established. |
| 3249 | 20374961 | Here, we show that mice lacking both leptin and insulin receptors in POMC neurons (Pomc-Cre, Lepr(flox/flox) IR(flox/flox) mice) display systemic insulin resistance, which is distinct from the single deletion of either receptor. |
| 3250 | 20374961 | We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function. |
| 3251 | 20374961 | Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. |
| 3252 | 20374961 | Circulating leptin and insulin convey information regarding energy stores to the central nervous system, particularly the hypothalamus. |
| 3253 | 20374961 | Hypothalamic pro-opiomelanocortin (POMC) neurons regulate energy balance and glucose homeostasis and express leptin and insulin receptors. |
| 3254 | 20374961 | However, the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established. |
| 3255 | 20374961 | Here, we show that mice lacking both leptin and insulin receptors in POMC neurons (Pomc-Cre, Lepr(flox/flox) IR(flox/flox) mice) display systemic insulin resistance, which is distinct from the single deletion of either receptor. |
| 3256 | 20374961 | We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function. |
| 3257 | 20472052 | We evaluated arginine vasopressin (AVP), glucocorticoid receptor (GR), and corticotropin-releasing hormone (CRH) expression with immunohistochemistry (IHC), immunofluorescence, real-time PCR, and Western blot analysis in each treatment group 7 weeks post ADX to assess HPA axis regulatory patterns in connection with type 2 diabetes. |
| 3258 | 20472052 | Additionally, mRNA expression of AVP and CRH receptors (V1aR, V1bR, CRHR1, and CRHR2) was also measured and adrenocorticotropin hormone (ACTH) immunoreactivity was surveyed by IHC to add to data regarding the regulatory mechanism. |
| 3259 | 20472052 | Without the negative feedback system of corticosterone, CRH is highly enhanced and may primarily combine with CRHR1 to stimulate negative feedback through ACTH in the pituitary gland in type 2 diabetic rats with long-term ADX. |
| 3260 | 20472052 | We evaluated arginine vasopressin (AVP), glucocorticoid receptor (GR), and corticotropin-releasing hormone (CRH) expression with immunohistochemistry (IHC), immunofluorescence, real-time PCR, and Western blot analysis in each treatment group 7 weeks post ADX to assess HPA axis regulatory patterns in connection with type 2 diabetes. |
| 3261 | 20472052 | Additionally, mRNA expression of AVP and CRH receptors (V1aR, V1bR, CRHR1, and CRHR2) was also measured and adrenocorticotropin hormone (ACTH) immunoreactivity was surveyed by IHC to add to data regarding the regulatory mechanism. |
| 3262 | 20472052 | Without the negative feedback system of corticosterone, CRH is highly enhanced and may primarily combine with CRHR1 to stimulate negative feedback through ACTH in the pituitary gland in type 2 diabetic rats with long-term ADX. |
| 3263 | 20493223 | In adult handled males (90-days old) we find not only POMC-derived hormones alterations (enhanced basal plasma corticosterone (+91%) and ACTH (+109%)) but also overweight (+5.4%), fasting hyperglycemia (+40%), hypertriglyceridemia (+21%), enhanced brain mRNA expression of hydroxysteroid(11-beta)dehydrogenase type-1 (HSD11B1) (+49%), and decreased mRNA-HSD11B2 (-39%). |
| 3264 | 20558893 | CT scan of the chest showed two nodular lesions in the right lung (S5, S7), while a mild uptake was noted only in S5 lesion by FDG-PET, but positive uptake was only in S7 lesion by somatostatin receptor scintigraphy (SRS). |
| 3265 | 20558893 | Inferior petrosal sinus sampling revealed a gradient of plasma ACTH after CRH stimulation, consistent with the diagnosis of Cushing' s disease. |
| 3266 | 20558893 | This was a diagnostic challenging case with ectopic ACTH syndrome indistinguishable from Cushing' s disease by various endocrine and imaging tests, among which SRS successfully localized the tumor responsible for ectopic ACTH secretion. |
| 3267 | 20558893 | CT scan of the chest showed two nodular lesions in the right lung (S5, S7), while a mild uptake was noted only in S5 lesion by FDG-PET, but positive uptake was only in S7 lesion by somatostatin receptor scintigraphy (SRS). |
| 3268 | 20558893 | Inferior petrosal sinus sampling revealed a gradient of plasma ACTH after CRH stimulation, consistent with the diagnosis of Cushing' s disease. |
| 3269 | 20558893 | This was a diagnostic challenging case with ectopic ACTH syndrome indistinguishable from Cushing' s disease by various endocrine and imaging tests, among which SRS successfully localized the tumor responsible for ectopic ACTH secretion. |
| 3270 | 20626417 | Possible interactions between neuropeptide Y (NPY), agouti-related protein (AGRP), α-melanocyte-stimulating hormone (MSH) and corticotropin-releasing hormone (CRH) were evaluated in an in vitro hypothalamic explant system. |
| 3271 | 20626417 | Incubation of hypothalamic explants with 0.4, 4 and 40 nmol/L CART (55-102) for 45 min significantly increased NPY IR, whereas exposure of explants to 4 nmol/L CART (55-102) increased AGRP IR and CRH IR. |
| 3272 | 20668022 | At P16, LL DIO neonates had increased arcuate nucleus (ARC) binding of leptin to its extracellular receptors and at P28 an associated increase of their agouti-related peptide and alpha-MSH axonal projections to the paraventricular nucleus. |
| 3273 | 20668022 | Reduced body weight persisted and was associated with increased ARC leptin receptor binding and sensitivity to the anorectic effects of leptin, reduced adiposity, and enhanced insulin sensitivity in LL DIO rats fed chow until 10 wk of age. |
| 3274 | 20694162 | Recently, we serendipitously discovered that mice with the deficiency of the enzyme prolylcarboxypeptidase (PRCP) have elevated alpha-melanocyte-stimulating hormone (alpha-MSH) levels which lead to decreased food intake and weight loss. |
| 3275 | 20694162 | This suggests that PRCP is an endogenous inactivator of alpha-MSH and an appetite stimulant. |
| 3276 | 20694162 | The discovery of a new biological activity of PRCP in the PRCP-deficient mice and studies of alpha-MSH function indicate the importance and complexity of the hypothalamic pro-opiomelanocortin (POMC) system in altering food intake. |
| 3277 | 20694162 | Identifying a role for PRCP in regulating alpha-MSH in the brain may be a critical step in enhancing our understanding of how the brain controls food intake and body weight. |
| 3278 | 20694162 | Recently, we serendipitously discovered that mice with the deficiency of the enzyme prolylcarboxypeptidase (PRCP) have elevated alpha-melanocyte-stimulating hormone (alpha-MSH) levels which lead to decreased food intake and weight loss. |
| 3279 | 20694162 | This suggests that PRCP is an endogenous inactivator of alpha-MSH and an appetite stimulant. |
| 3280 | 20694162 | The discovery of a new biological activity of PRCP in the PRCP-deficient mice and studies of alpha-MSH function indicate the importance and complexity of the hypothalamic pro-opiomelanocortin (POMC) system in altering food intake. |
| 3281 | 20694162 | Identifying a role for PRCP in regulating alpha-MSH in the brain may be a critical step in enhancing our understanding of how the brain controls food intake and body weight. |
| 3282 | 20694162 | Recently, we serendipitously discovered that mice with the deficiency of the enzyme prolylcarboxypeptidase (PRCP) have elevated alpha-melanocyte-stimulating hormone (alpha-MSH) levels which lead to decreased food intake and weight loss. |
| 3283 | 20694162 | This suggests that PRCP is an endogenous inactivator of alpha-MSH and an appetite stimulant. |
| 3284 | 20694162 | The discovery of a new biological activity of PRCP in the PRCP-deficient mice and studies of alpha-MSH function indicate the importance and complexity of the hypothalamic pro-opiomelanocortin (POMC) system in altering food intake. |
| 3285 | 20694162 | Identifying a role for PRCP in regulating alpha-MSH in the brain may be a critical step in enhancing our understanding of how the brain controls food intake and body weight. |
| 3286 | 20694162 | Recently, we serendipitously discovered that mice with the deficiency of the enzyme prolylcarboxypeptidase (PRCP) have elevated alpha-melanocyte-stimulating hormone (alpha-MSH) levels which lead to decreased food intake and weight loss. |
| 3287 | 20694162 | This suggests that PRCP is an endogenous inactivator of alpha-MSH and an appetite stimulant. |
| 3288 | 20694162 | The discovery of a new biological activity of PRCP in the PRCP-deficient mice and studies of alpha-MSH function indicate the importance and complexity of the hypothalamic pro-opiomelanocortin (POMC) system in altering food intake. |
| 3289 | 20694162 | Identifying a role for PRCP in regulating alpha-MSH in the brain may be a critical step in enhancing our understanding of how the brain controls food intake and body weight. |
| 3290 | 20703054 | However, aging did not alter hypothalamic expression of key anorexigens, alpha-MSH and CART. |
| 3291 | 20713347 | Reduction of false-negative results in inferior petrosal sinus sampling with simultaneous prolactin and corticotropin measurement. |
| 3292 | 20855609 | Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice. |
| 3293 | 20855609 | Leptin monotherapy reverses the deadly consequences and improves several of the metabolic imbalances caused by insulin-deficient type 1 diabetes (T1D) in rodents. |
| 3294 | 20855609 | Here, we report that intracerebroventricular (icv) infusion of leptin reverses lethality and greatly improves hyperglycemia, hyperglucagonemia, hyperketonemia, and polyuria caused by insulin deficiency in mice. |
| 3295 | 20855609 | Also, icv leptin delivery improves expression of the metabolically relevant hypothalamic neuropeptides proopiomelanocortin, neuropeptide Y, and agouti-related peptide in T1D mice. |
| 3296 | 20855609 | Pancreatic β-cell regeneration does not underlie these beneficial effects of leptin, because circulating insulin levels were undetectable at basal levels and following a glucose overload. |
| 3297 | 20886012 | Girls with slowly progressive precocious breast development, who were overweight and had PA (SPPOPA, 6.2-8.2 years, n = 5), overweight PA (6.6-10.8 years, n = 7), and overweight premenarcheal controls (OW-PUB, 10.6-12.8 years, n = 8) underwent hormonal sleep testing and GnRH agonist (GnRHag) and ACTH tests. |
| 3298 | 20948526 | Quantification of proopiomelanocortin (POMC) and neuropeptide-Y (NPY) populations in the arcuate nucleus of the hypothalamus (ARH) of offspring of wild-type vs. |
| 3299 | 20953065 | GH secretion is mainly regulated at the hypothalamus by a dual interplay between growth hormone releasing hormone (GHRH) and somatostatin, which are modulated by various factors. |
| 3300 | 20953065 | We examined the regulatory mechanism of GH secretion in an apparently healthy young man without decreased IGF-1 concentration and nocturnal GH secretion, but who showed low responses to insulin tolerance (ITT) and to GHRP-2 tests. |
| 3301 | 20953065 | However, he had normal secretion of pituitary hormone based on hypothalamic releasing hormone tests combined with CRH, GRH as GHRH, LH-RH and TRH. |
| 3302 | 20953065 | In addition, he had a GH response without paradoxical secretion to TRH stimulation as well as an ACTH response to subcutaneous glucagon stimulation, and AVP secretion responded to 5% hypertonic saline infusion, though it was not adequately stimulated by ITT. |
| 3303 | 21083697 | Several central and peripheral neurohumoral factors (the major ones being the anorectic adipokines leptin and adiponecin and the orexigenic gut hormone ghrelin) acting on the anorectic (pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript) and orexigenic (neuropeptide Y and agouti gene-related protein) neurons regulate energy balance. |
| 3304 | 21132537 | Genotyping of all coding exons of HESX1, LHX4, PROP1, POU1F1 and GH1 genes were performed according to a diagnostic algorithm based on clinical, hormonal and neuroradiological phenotype. |
| 3305 | 21132537 | Among two sibling pairs, one pair that presented with complete anterior pituitary insufficiency, had a compound heterozygous PROP1 gene mutation (codons 117 and 120: exon 3 p Phe 117 Ile (c349 T>A) and p Arg 120 Cys (c358 C>T)) with a phenotype of very late onset ACTH-insufficiency. |
| 3306 | 21324829 | Corticotropin-independent macronodular adrenal hyperplasia associated with insulinoma. |
| 3307 | 21415158 | In ESRD, the neurohormone arginine vasopressin (AVP) may act primarily through V1a and V1b receptors, which promote vasoconstriction, myocardial hypertrophy, and release of adrenocorticotropic hormone. |
| 3308 | 21536883 | Here, we generated germline transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targeted to the adenohypophyseal proopiomelanocortin (POMC) lineage, which recapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resistance. |
| 3309 | 21536883 | Molecular analyses in vitro and in vivo showed that R-roscovitine suppresses ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit by up-regulating p27, p21 and p57, and downregulates cyclin E expression. |
| 3310 | 21536883 | Here, we generated germline transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targeted to the adenohypophyseal proopiomelanocortin (POMC) lineage, which recapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resistance. |
| 3311 | 21536883 | Molecular analyses in vitro and in vivo showed that R-roscovitine suppresses ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit by up-regulating p27, p21 and p57, and downregulates cyclin E expression. |
| 3312 | 21565670 | A chimeric gene duplication leads to ectopic aldosterone synthase activity in the cortisol-producing zona fasciculata of the adrenal cortex, under the regulation of adrenocorticotropin (ACTH). |
| 3313 | 21565670 | Glucocorticoid suppression of ACTH is the mainstay of treatment; alternative treatments include mineralocorticoid receptor antagonists. |
| 3314 | 21565670 | A chimeric gene duplication leads to ectopic aldosterone synthase activity in the cortisol-producing zona fasciculata of the adrenal cortex, under the regulation of adrenocorticotropin (ACTH). |
| 3315 | 21565670 | Glucocorticoid suppression of ACTH is the mainstay of treatment; alternative treatments include mineralocorticoid receptor antagonists. |
| 3316 | 21593429 | The present study employed a rat model of insulin-induced RHG spanning postnatal days (P)24-28, a neurodevelopmental equivalent of early childhood in humans, to assess the long-term effects on mRNA levels for proteins relevant to the LHPA function and the corticosterone responses to ACTH stimulation of dispersed adrenocortical cells in vitro and restraint stress in vivo at adulthood. |
| 3317 | 21593429 | This early RHG model resulted in a hyporesponsive LHPA axis characterized by impaired corticosterone response, increased hippocampal glucocorticoid and mineralocorticoid receptor (GR and MR), decreased hypothalamic corticotropin-releasing hormone, increased adrenal steroidogenic-acute-regulatory protein and GR, and decreased adrenal MR, melanocortin-type-2 receptor and low-density lipoprotein receptor expression. |
| 3318 | 21769255 | His endocrinological examination revealed low levels of plasma adrenocorticotropic hormone (ACTH) and cortisol, and a normal response of ACTH to the corticotrophin-releasing hormone (CRH) challenge. |
| 3319 | 21769255 | Plasma ACTH did not increase with insulin loading. |
| 3320 | 21769255 | His endocrinological examination revealed low levels of plasma adrenocorticotropic hormone (ACTH) and cortisol, and a normal response of ACTH to the corticotrophin-releasing hormone (CRH) challenge. |
| 3321 | 21769255 | Plasma ACTH did not increase with insulin loading. |
| 3322 | 21777182 | Beside the large family A (rhodopsin-like receptors) and family C GPCR (metabotropic glutamate receptors), the small family B1 GPCR (secretin-like receptors) includes important receptors such as vasoactive intestinal peptide receptors (VPAC), pituitary adenylyl cyclase activating peptide receptor (PAC1R), secretin receptor (SECR), growth hormone releasing factor receptor (GRFR), glucagon receptor (GCGR), glucagon like-peptide 1 and 2 receptors (GLPR), gastric inhibitory peptide receptor (GIPR), parathyroid hormone receptors (PTHR), calcitonin receptors (CTR) and corticotropin-releasing factor receptors (CRFR). |
| 3323 | 21873226 | In addition, leptin-treated animals exhibited marked improvement of insulin sensitivity and glucose homeostasis compared with controls, whereas pancreatic insulin content was 50% higher in leptin-treated animals (P < 0.05). |
| 3324 | 21873226 | These effects coincided with activation of leptin and insulin signaling pathways and down-regulation of the PKR-like endoplasmic reticulum (ER) kinase/eukaryotic translation inhibition factor 2α (PERK-eIF2α) arm of ER stress in liver, skeletal muscle, and adipose tissue as well as increased pro-opiomelanocortin and decreased agouti-related peptide in the hypothalamus. |
| 3325 | 21873226 | In contrast, several markers of inflammation/immune function were elevated with leptin treatment in the same tissues (P < 0.05), suggesting that the leptin-mediated increase of insulin sensitivity was not attributable to decreased inflammation. |
| 3326 | 21873226 | Thus, leptin administration improves insulin sensitivity and normalizes fasting plasma glucose in diabetic UCD-T2DM rats, independent of energy intake, via peripheral and possibly centrally mediated actions, in part by decreasing circulating glucagon and ER stress. |
| 3327 | 21980299 | The most significantly associated SNP (rs539514, P = 5.66×10⁻¹¹) resides in an intronic region of the LMO7 (LIM domain only 7) gene on 13q22. |
| 3328 | 21980299 | The second most significantly associated SNP (rs478222, P = 3.50×10⁻⁹ resides in an intronic region of the EFR3B (protein EFR3 homolog B) gene on 2p23; however, the region of linkage disequilibrium is approximately 800 kb and harbors additional multiple genes, including NCOA1, C2orf79, CENPO, ADCY3, DNAJC27, POMC, and DNMT3A. |
| 3329 | 21980299 | The third most significantly associated SNP (rs924043, P = 8.06×10⁻⁹ lies in an intergenic region on 6q27, where the region of association is approximately 900 kb and harbors multiple genes including WDR27, C6orf120, PHF10, TCTE3, C6orf208, LOC154449, DLL1, FAM120B, PSMB1, TBP, and PCD2. |
| 3330 | 22057966 | Growth hormone deficiency and disturbances in puberty are the most common, but children can also experience ACTH deficiency, diabetes insipidus, central hypothyroidism, and elevated prolactin. |
| 3331 | 22100407 | NPY and MC4R signaling regulate thyroid hormone levels during fasting through both central and peripheral pathways. |
| 3332 | 22100407 | Previous studies demonstrate that leptin communicates nutritional status to the HPT axis through thyrotropin-releasing hormone (TRH) in the paraventricular nucleus (PVN) of the hypothalamus. |
| 3333 | 22100407 | Leptin targets TRH neurons either directly or indirectly via the arcuate nucleus through pro-opiomelanocortin (POMC) and agouti-related peptide/neuropeptide Y (AgRP/NPY) neurons. |
| 3334 | 22100407 | To evaluate the role of these pathways in vivo, we developed double knockout mice that lack both the melanocortin 4 receptor (MC4R) and NPY. |
| 3335 | 22100407 | We show that NPY is required for fasting-induced suppression of Trh expression in the PVN. |
| 3336 | 22100407 | However, both MC4R and NPY are required for activation of hepatic pathways that metabolize T(4) during the fasting response. |
| 3337 | 22210743 | Differential insulin receptor substrate-1 (IRS1)-related modulation of neuropeptide Y and proopiomelanocortin expression in nondiabetic and diabetic IRS2-/- mice. |
| 3338 | 22210743 | Insulin resistance and type 2 diabetes correlate with impaired leptin and insulin signaling. |
| 3339 | 22210743 | Our aim was to analyze how leptin and insulin signaling may differentially affect the expression of hypothalamic neuropeptides regulating food intake and hypothalamic inflammation in diabetic (D) and nondiabetic (ND) IRS2(-/-) mice. |
| 3340 | 22210743 | We analyzed the activation of leptin and insulin targets by Western blotting and their association by immunoprecipitation, as well as the mRNA levels of neuropeptide Y (NPY), proopiomelanocortin, and inflammatory markers by real-time PCR and colocalization of forkhead box protein O1 (FOXO1) and NPY by double immunohistochemistry in the hypothalamus. |
| 3341 | 22210743 | Serum leptin and insulin levels and hypothalamic Janus kinase 2 and signal transducer and activator of transcription factor 3 activation were increased in ND IRS2(-/-) mice. |
| 3342 | 22210743 | IRS1 levels and its association with Janus kinase 2 and p85 and protein kinase B activation were increased in ND IRS2(-/-). |
| 3343 | 22210743 | Increased FOXO1 positively correlated with NPY mRNA levels in D IRS2(-/-) mice, with FOXO1 showing mainly nuclear localization in D IRS2(-/-) and cytoplasmic in ND IRS2(-/-) mice. |
| 3344 | 22210743 | In conclusion, differential activation of these pathways and changes in the expression of NPY and inflammation may exert a protective effect against hypothalamic deregulation of appetite, suggesting that manipulation of these targets could be of interest in the treatment of insulin resistance and type 2 diabetes. |
| 3345 | 22210743 | Differential insulin receptor substrate-1 (IRS1)-related modulation of neuropeptide Y and proopiomelanocortin expression in nondiabetic and diabetic IRS2-/- mice. |
| 3346 | 22210743 | Insulin resistance and type 2 diabetes correlate with impaired leptin and insulin signaling. |
| 3347 | 22210743 | Our aim was to analyze how leptin and insulin signaling may differentially affect the expression of hypothalamic neuropeptides regulating food intake and hypothalamic inflammation in diabetic (D) and nondiabetic (ND) IRS2(-/-) mice. |
| 3348 | 22210743 | We analyzed the activation of leptin and insulin targets by Western blotting and their association by immunoprecipitation, as well as the mRNA levels of neuropeptide Y (NPY), proopiomelanocortin, and inflammatory markers by real-time PCR and colocalization of forkhead box protein O1 (FOXO1) and NPY by double immunohistochemistry in the hypothalamus. |
| 3349 | 22210743 | Serum leptin and insulin levels and hypothalamic Janus kinase 2 and signal transducer and activator of transcription factor 3 activation were increased in ND IRS2(-/-) mice. |
| 3350 | 22210743 | IRS1 levels and its association with Janus kinase 2 and p85 and protein kinase B activation were increased in ND IRS2(-/-). |
| 3351 | 22210743 | Increased FOXO1 positively correlated with NPY mRNA levels in D IRS2(-/-) mice, with FOXO1 showing mainly nuclear localization in D IRS2(-/-) and cytoplasmic in ND IRS2(-/-) mice. |
| 3352 | 22210743 | In conclusion, differential activation of these pathways and changes in the expression of NPY and inflammation may exert a protective effect against hypothalamic deregulation of appetite, suggesting that manipulation of these targets could be of interest in the treatment of insulin resistance and type 2 diabetes. |
| 3353 | 22223754 | This study used sheep to examine the effect of moderate maternal undernutrition (60 d before to 30 d after mating) and twinning to investigate changes in the key metabolic regulators proopiomelanocortin (POMC) and the glucocorticoid receptor (GR) in fetal hypothalami. |
| 3354 | 22246489 | The levels of all the pituitary hormones were elevated in response to a mixture of exogenous corticotrophin-releasing hormone (CRH), luteinizing hormone-releasing hormone (LH-RH), thyrotropin-releasing hormone (TRH), and growth hormone-releasing hormone (GRH). |
| 3355 | 22246489 | However, there was no response of ACTH and GH release to insulin-induced hypoglycemia and no response of LH and FSH release to clomiphene. |
| 3356 | 22276206 | Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity. |
| 3357 | 22276206 | Diet-induced obesity (DIO) in rodents is characterized by impaired activation of signal-transducer and activator of transcription 3 (STAT3) by leptin receptors (LepRb) within the hypothalamic arcuate nucleus. |
| 3358 | 22276206 | However, the neuro-chemical identity of the leptin-STAT3 resistant arcuate neurons has not been determined and the underlying mechanisms responsible for development of cellular leptin resistance remain unclear. |
| 3359 | 22276206 | To investigate this, we first measured arcuate gene expression of known key signaling components of the LepRb signaling pathway and tested whether specifically the critical arcuate pro-opiomelanocortin (POMC) neurons are resistant to LepRb-STAT3 signaling in mice given a high-fat-diet (HFD) compared to mice provided a low-fat control diet (LFD). |
| 3360 | 22276206 | We found that leptin-dependent STAT3 phosphorylation was decreased within POMC neurons of HFD mice. |
| 3361 | 22276206 | To investigate whether increased LepRb expression per se in POMC neurons can influence development of DIO and Socs3 expression, we created mice that over-express LepRb selectively in POMC neurons (POMC-LepRb). |
| 3362 | 22276206 | These data show that specifically POMC neurons of DIO mice are resistant to STAT3 activation by leptin, indicating that those cells might play a role in development of DIO. |
| 3363 | 22276206 | Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity. |
| 3364 | 22276206 | Diet-induced obesity (DIO) in rodents is characterized by impaired activation of signal-transducer and activator of transcription 3 (STAT3) by leptin receptors (LepRb) within the hypothalamic arcuate nucleus. |
| 3365 | 22276206 | However, the neuro-chemical identity of the leptin-STAT3 resistant arcuate neurons has not been determined and the underlying mechanisms responsible for development of cellular leptin resistance remain unclear. |
| 3366 | 22276206 | To investigate this, we first measured arcuate gene expression of known key signaling components of the LepRb signaling pathway and tested whether specifically the critical arcuate pro-opiomelanocortin (POMC) neurons are resistant to LepRb-STAT3 signaling in mice given a high-fat-diet (HFD) compared to mice provided a low-fat control diet (LFD). |
| 3367 | 22276206 | We found that leptin-dependent STAT3 phosphorylation was decreased within POMC neurons of HFD mice. |
| 3368 | 22276206 | To investigate whether increased LepRb expression per se in POMC neurons can influence development of DIO and Socs3 expression, we created mice that over-express LepRb selectively in POMC neurons (POMC-LepRb). |
| 3369 | 22276206 | These data show that specifically POMC neurons of DIO mice are resistant to STAT3 activation by leptin, indicating that those cells might play a role in development of DIO. |
| 3370 | 22276206 | Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity. |
| 3371 | 22276206 | Diet-induced obesity (DIO) in rodents is characterized by impaired activation of signal-transducer and activator of transcription 3 (STAT3) by leptin receptors (LepRb) within the hypothalamic arcuate nucleus. |
| 3372 | 22276206 | However, the neuro-chemical identity of the leptin-STAT3 resistant arcuate neurons has not been determined and the underlying mechanisms responsible for development of cellular leptin resistance remain unclear. |
| 3373 | 22276206 | To investigate this, we first measured arcuate gene expression of known key signaling components of the LepRb signaling pathway and tested whether specifically the critical arcuate pro-opiomelanocortin (POMC) neurons are resistant to LepRb-STAT3 signaling in mice given a high-fat-diet (HFD) compared to mice provided a low-fat control diet (LFD). |
| 3374 | 22276206 | We found that leptin-dependent STAT3 phosphorylation was decreased within POMC neurons of HFD mice. |
| 3375 | 22276206 | To investigate whether increased LepRb expression per se in POMC neurons can influence development of DIO and Socs3 expression, we created mice that over-express LepRb selectively in POMC neurons (POMC-LepRb). |
| 3376 | 22276206 | These data show that specifically POMC neurons of DIO mice are resistant to STAT3 activation by leptin, indicating that those cells might play a role in development of DIO. |
| 3377 | 22276206 | Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity. |
| 3378 | 22276206 | Diet-induced obesity (DIO) in rodents is characterized by impaired activation of signal-transducer and activator of transcription 3 (STAT3) by leptin receptors (LepRb) within the hypothalamic arcuate nucleus. |
| 3379 | 22276206 | However, the neuro-chemical identity of the leptin-STAT3 resistant arcuate neurons has not been determined and the underlying mechanisms responsible for development of cellular leptin resistance remain unclear. |
| 3380 | 22276206 | To investigate this, we first measured arcuate gene expression of known key signaling components of the LepRb signaling pathway and tested whether specifically the critical arcuate pro-opiomelanocortin (POMC) neurons are resistant to LepRb-STAT3 signaling in mice given a high-fat-diet (HFD) compared to mice provided a low-fat control diet (LFD). |
| 3381 | 22276206 | We found that leptin-dependent STAT3 phosphorylation was decreased within POMC neurons of HFD mice. |
| 3382 | 22276206 | To investigate whether increased LepRb expression per se in POMC neurons can influence development of DIO and Socs3 expression, we created mice that over-express LepRb selectively in POMC neurons (POMC-LepRb). |
| 3383 | 22276206 | These data show that specifically POMC neurons of DIO mice are resistant to STAT3 activation by leptin, indicating that those cells might play a role in development of DIO. |
| 3384 | 22276206 | Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity. |
| 3385 | 22276206 | Diet-induced obesity (DIO) in rodents is characterized by impaired activation of signal-transducer and activator of transcription 3 (STAT3) by leptin receptors (LepRb) within the hypothalamic arcuate nucleus. |
| 3386 | 22276206 | However, the neuro-chemical identity of the leptin-STAT3 resistant arcuate neurons has not been determined and the underlying mechanisms responsible for development of cellular leptin resistance remain unclear. |
| 3387 | 22276206 | To investigate this, we first measured arcuate gene expression of known key signaling components of the LepRb signaling pathway and tested whether specifically the critical arcuate pro-opiomelanocortin (POMC) neurons are resistant to LepRb-STAT3 signaling in mice given a high-fat-diet (HFD) compared to mice provided a low-fat control diet (LFD). |
| 3388 | 22276206 | We found that leptin-dependent STAT3 phosphorylation was decreased within POMC neurons of HFD mice. |
| 3389 | 22276206 | To investigate whether increased LepRb expression per se in POMC neurons can influence development of DIO and Socs3 expression, we created mice that over-express LepRb selectively in POMC neurons (POMC-LepRb). |
| 3390 | 22276206 | These data show that specifically POMC neurons of DIO mice are resistant to STAT3 activation by leptin, indicating that those cells might play a role in development of DIO. |
| 3391 | 22486586 | Treatment with selective 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) inhibitors could be a therapeutic strategy in paediatric patients with manifestations of the metabolic syndrome. |
| 3392 | 22486586 | The effect of 11β-HSD1 treatment in children on bone differentiation and development as well as adrenocorticotropic hormone (ACTH), circulating and local cortisol tissue concentrations, androgens and respective stress response is not yet known. |
| 3393 | 22592190 | A surge of corticotropin and cortisol, 19.4 pmol/L and 712.1 nmol/L respectively, was found on Day 5 when luteinizing hormone, follicle stimulating hormone, and testosterone were subnormal and prolactin was slightly elevated. |
| 3394 | 22592190 | Subsequently, corticotropin and cortisol levels normalized together with normalization of luteinizing hormone, follicle stimulating hormone, anti-diuretic hormone, thyroid stimulating hormone, prolactin, testosterone and thyroid hormone levels. |
| 3395 | 22592190 | A surge of corticotropin and cortisol, 19.4 pmol/L and 712.1 nmol/L respectively, was found on Day 5 when luteinizing hormone, follicle stimulating hormone, and testosterone were subnormal and prolactin was slightly elevated. |
| 3396 | 22592190 | Subsequently, corticotropin and cortisol levels normalized together with normalization of luteinizing hormone, follicle stimulating hormone, anti-diuretic hormone, thyroid stimulating hormone, prolactin, testosterone and thyroid hormone levels. |
| 3397 | 22663897 | CUMS procedure significantly up-regulated corticotropin-releasing factor (CRF)-related peptide urocortin 2 expression and elevated cAMP production, resulting in over-expression of suppressor of cytokine signaling 3 (SOCS3) in hypothalamic arcuate nucleus (ARC) of rats. |
| 3398 | 22663897 | Furthermore, SOCS3 activation blocked insulin signaling pathway through the suppression of insulin receptor substrate 2 (IRS2) phosphotyrosine and phosphatidylinositol-3-kinase (PI3-K) activation in hypothalamic ARC of CUMS rats after high-level of insulin stimulation. |
| 3399 | 22700769 | In addition, a large number of refeeding-activated c-Fos-expressing neurons were observed in the lateral parvocellular subdivision (PVNl) that also contained CTB and were innervated by axon terminals of proopiomelanocortin neurons. |
| 3400 | 22707647 | Other findings included an absent cortisol response to corticotropin stimulation, presence of serum anti-21-hydroxylase antibodies, and mononuclear cell infiltration--consistent with adrenalitis. |
| 3401 | 22789859 | Plasma concentrations of thyroid-stimulating hormone, thyroxine, growth hormone (GH) and insulin-like growth factor-1 were decreased; plasma adrenocorticotropic hormone (ACTH) was slightly elevated and plasma α-melanocyte-stimulating hormone (MSH) was within the reference range. |
| 3402 | 22790131 | Usefulness and limitations of unilateral adrenalectomy for ACTH-independent macronodular adrenal hyperplasia in a patient with poor glycemic control. |
| 3403 | 22790131 | Adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a rare disease which causes Cushing's syndrome. |
| 3404 | 22790131 | Usefulness and limitations of unilateral adrenalectomy for ACTH-independent macronodular adrenal hyperplasia in a patient with poor glycemic control. |
| 3405 | 22790131 | Adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is a rare disease which causes Cushing's syndrome. |
| 3406 | 22796301 | Genetic variants in the transcription factor 7-like 2(Tcf7l2) gene have been found to confer a significant risk of type 2 diabetes and attenuated insulin secretion. |
| 3407 | 22796301 | TCF was also found co-localized with peptides that regulate energy homeostasis including AgRP, POMC and NPY. |
| 3408 | 22796301 | TCF7l2, some variants of which have been shown to impair GLP-1-induced insulin secretion, was also found co-localize with GLP-1 in adult TCF wild type progeny. |
| 3409 | 22848202 | In animal studies this has been linked with abnormal hypothalamic gene expression of appetite regulators such as downregulation of NPY and POMC in the arcuate nucleus of the hypothalamus. |
| 3410 | 22941110 | We found that Rho-kinase 1 (ROCK1) regulates leptin action on body weight homeostasis by activating JAK2, an initial trigger of leptin receptor signaling. |
| 3411 | 22941110 | Leptin promoted the physical interaction of JAK2 and ROCK1, thereby increasing phosphorylation of JAK2 and downstream activation of Stat3 and FOXO1. |
| 3412 | 22941110 | Mice lacking ROCK1 in either pro-opiomelanocortin (POMC) or agouti-related protein neurons, mediators of leptin action, displayed obesity and impaired leptin sensitivity. |
| 3413 | 22941110 | Notably, ROCK1 was a specific mediator of leptin, but not insulin, regulation of POMC neuronal activity. |
| 3414 | 22941110 | We found that Rho-kinase 1 (ROCK1) regulates leptin action on body weight homeostasis by activating JAK2, an initial trigger of leptin receptor signaling. |
| 3415 | 22941110 | Leptin promoted the physical interaction of JAK2 and ROCK1, thereby increasing phosphorylation of JAK2 and downstream activation of Stat3 and FOXO1. |
| 3416 | 22941110 | Mice lacking ROCK1 in either pro-opiomelanocortin (POMC) or agouti-related protein neurons, mediators of leptin action, displayed obesity and impaired leptin sensitivity. |
| 3417 | 22941110 | Notably, ROCK1 was a specific mediator of leptin, but not insulin, regulation of POMC neuronal activity. |
| 3418 | 22966070 | Tub has a key role in insulin and leptin signaling and action in vivo in hypothalamic nuclei. |
| 3419 | 22966070 | In the current study, we investigated whether insulin, leptin, and obesity can modulate Tub in vivo in hypothalamic nuclei, and we investigated possible consequences on energy balance, neuropeptide expression, and hepatic glucose metabolism. |
| 3420 | 22966070 | Food intake, metabolic characteristics, signaling proteins, and neuropeptide expression were measured in response to fasting and refeeding, intracerebroventricular insulin and leptin, and Tub antisense oligonucleotide (ASO). |
| 3421 | 22966070 | Tub is a substrate of insulin receptor tyrosine kinase (IRTK) and leptin receptor (LEPR)-Janus kinase 2 (JAK2) in hypothalamic nuclei. |
| 3422 | 22966070 | After leptin or insulin stimulation, Tub translocates to the nucleus. |
| 3423 | 22966070 | Inhibition of Tub expression in hypothalamus by ASO increased food intake, fasting blood glucose, and hepatic glucose output, decreased O(2) consumption, and blunted the effect of insulin or leptin on proopiomelanocortin, thyroid-releasing hormone, melanin-concentrating hormone, and orexin expression. |
| 3424 | 22966070 | In hypothalamus of mice administered a high-fat diet, there is a reduction in leptin and insulin-induced Tub-p-tyr and nuclear translocation, which is reversed by reducing protein tyrosine phosphatase 1B expression. |
| 3425 | 22966070 | These results indicate that Tub has a key role in the control of insulin and leptin effects on food intake, and the modulation of Tub may contribute to insulin and leptin resistance in DIO mice. |
| 3426 | 23011322 | For functional adenoma, remission rates were 30/41 (73%) for GH-secreting, 12/12 (100%) for ACTH-secreting, and 8/17 (47%) for prolactin-secreting tumors. |
| 3427 | 23045190 | Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTH-corticosterone system hyper-functioning. |
| 3428 | 23064477 | Combined anterior pituitary stimulation test and insulin-induced hypoglycemic test confirmed the diagnosis of panhypopituitarism, including adrenocortical insufficiency due to pituitary and hypothalamic dysfunction by stalk compression. |
| 3429 | 23064477 | Synthesis of immature ACTH is generally thought to be due to impaired processing of the precursor proopiomelanocortin (POMC) through activation of prohormone convertase (PC)-1 by CRH. |
| 3430 | 23112343 | The principal effectors of the stress system are corticotropin-releasing hormone (CRH), arginine vasopressin, the proopiomelanocortin-derived peptides α-melanocyte-stimulating hormone and β-endorphin, the glucocorticoids, and the catecholamines norepinephrine and epinephrine. |
| 3431 | 23119079 | Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. |
| 3432 | 23119079 | Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. |
| 3433 | 23119079 | IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. |
| 3434 | 23119079 | This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. |
| 3435 | 23119079 | Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions. |
| 3436 | 23119079 | Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. |
| 3437 | 23119079 | Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. |
| 3438 | 23119079 | IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. |
| 3439 | 23119079 | This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. |
| 3440 | 23119079 | Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions. |
| 3441 | 23119079 | Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. |
| 3442 | 23119079 | Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. |
| 3443 | 23119079 | IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. |
| 3444 | 23119079 | This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. |
| 3445 | 23119079 | Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions. |
| 3446 | 23119079 | Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. |
| 3447 | 23119079 | Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. |
| 3448 | 23119079 | IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. |
| 3449 | 23119079 | This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. |
| 3450 | 23119079 | Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions. |
| 3451 | 23119079 | Female mice lacking leptin and insulin receptors in pro-opiomelanocortin neurons (IR/LepR(POMC) mice) and littermate controls were evaluated for estrous cyclicity, ovarian and adipose tissue morphology, and body composition by QMR and CT scan. |
| 3452 | 23119079 | Forty-five percent of IR/LepR(POMC) mice showed reduced or absent ovulation. |
| 3453 | 23119079 | IR/LepR(POMC) mice also had increased fat mass and adipocyte hypertrophy. |
| 3454 | 23119079 | This report is the first to show the presence of inflammation in IR/LepR(POMC) mice, which develop a PCOS-like phenotype. |
| 3455 | 23119079 | Thus, IR/LepR(POMC) mice may serve as a new mouse model to clarify the involvement of adipose and liver tissue in the pathogenesis and etiology of PCOS, allowing more targeted research on the development of PCOS and potential therapeutic interventions. |
| 3456 | 23161869 | AgRP innervation onto POMC neurons increases with age and is accelerated with chronic high-fat feeding in male mice. |
| 3457 | 23161869 | Hypothalamic neurons coexpressing agouti-related peptide (AgRP) and neuropeptide Y are direct leptin targets. |
| 3458 | 23161869 | We show here that AgRP and neuropeptide Y innvervation onto POMC neurons increases dramatically with age in male mice. |
| 3459 | 23161869 | Neuronal activity is significantly attenuated in POMC neurons that receive a high density of AgRP puncta. |
| 3460 | 23161869 | These high-density AgRP inputs correlate with leptin levels in normal mice and are nearly absent in mice lacking leptin. |
| 3461 | 23161869 | The progression of increased AgRP innervation onto POMC somas is accelerated in hyperleptinemic, diet-induced obese mice. |
| 3462 | 23161869 | Together our study suggests that modulation of hypothalamic AgRP innervation constitutes one mechanism to counter the effects of the age-associated rise in leptin levels, thus sustaining body weight and fat mass at an elevated level in adulthood. |
| 3463 | 23161869 | AgRP innervation onto POMC neurons increases with age and is accelerated with chronic high-fat feeding in male mice. |
| 3464 | 23161869 | Hypothalamic neurons coexpressing agouti-related peptide (AgRP) and neuropeptide Y are direct leptin targets. |
| 3465 | 23161869 | We show here that AgRP and neuropeptide Y innvervation onto POMC neurons increases dramatically with age in male mice. |
| 3466 | 23161869 | Neuronal activity is significantly attenuated in POMC neurons that receive a high density of AgRP puncta. |
| 3467 | 23161869 | These high-density AgRP inputs correlate with leptin levels in normal mice and are nearly absent in mice lacking leptin. |
| 3468 | 23161869 | The progression of increased AgRP innervation onto POMC somas is accelerated in hyperleptinemic, diet-induced obese mice. |
| 3469 | 23161869 | Together our study suggests that modulation of hypothalamic AgRP innervation constitutes one mechanism to counter the effects of the age-associated rise in leptin levels, thus sustaining body weight and fat mass at an elevated level in adulthood. |
| 3470 | 23161869 | AgRP innervation onto POMC neurons increases with age and is accelerated with chronic high-fat feeding in male mice. |
| 3471 | 23161869 | Hypothalamic neurons coexpressing agouti-related peptide (AgRP) and neuropeptide Y are direct leptin targets. |
| 3472 | 23161869 | We show here that AgRP and neuropeptide Y innvervation onto POMC neurons increases dramatically with age in male mice. |
| 3473 | 23161869 | Neuronal activity is significantly attenuated in POMC neurons that receive a high density of AgRP puncta. |
| 3474 | 23161869 | These high-density AgRP inputs correlate with leptin levels in normal mice and are nearly absent in mice lacking leptin. |
| 3475 | 23161869 | The progression of increased AgRP innervation onto POMC somas is accelerated in hyperleptinemic, diet-induced obese mice. |
| 3476 | 23161869 | Together our study suggests that modulation of hypothalamic AgRP innervation constitutes one mechanism to counter the effects of the age-associated rise in leptin levels, thus sustaining body weight and fat mass at an elevated level in adulthood. |
| 3477 | 23161869 | AgRP innervation onto POMC neurons increases with age and is accelerated with chronic high-fat feeding in male mice. |
| 3478 | 23161869 | Hypothalamic neurons coexpressing agouti-related peptide (AgRP) and neuropeptide Y are direct leptin targets. |
| 3479 | 23161869 | We show here that AgRP and neuropeptide Y innvervation onto POMC neurons increases dramatically with age in male mice. |
| 3480 | 23161869 | Neuronal activity is significantly attenuated in POMC neurons that receive a high density of AgRP puncta. |
| 3481 | 23161869 | These high-density AgRP inputs correlate with leptin levels in normal mice and are nearly absent in mice lacking leptin. |
| 3482 | 23161869 | The progression of increased AgRP innervation onto POMC somas is accelerated in hyperleptinemic, diet-induced obese mice. |
| 3483 | 23161869 | Together our study suggests that modulation of hypothalamic AgRP innervation constitutes one mechanism to counter the effects of the age-associated rise in leptin levels, thus sustaining body weight and fat mass at an elevated level in adulthood. |
| 3484 | 23169787 | However, there was no effect of insulin treatment on total food intake nor on hypothalamic neuropeptide Y or proopiomelanocortin mRNA expression, and insulin-treated animals did not become insulin-resistant. |
| 3485 | 23196783 | We investigated whether common GR genes (ER22/23EK, N363S, Bcl I, and 9β) and adrenocorticotropin receptor promoter polymorphisms influence susceptibility for unilateral adrenal incidentaloma (AI), plus GR and Hsp expression in tumorous (n = 19), peritumorous (n = 13) and normal adrenocortical (n = 11) tissues. |
| 3486 | 23228667 | One of the medical treatments used in Cushing's disease is the somatostatin analogue pasireotide, which acts on adrenocorticotropic hormone (ACTH) secretion by the pituitary. |
| 3487 | 23235923 | Control of CYP11B2/CYP11B1 expression ratio and consequences for the zonation of the adrenal cortex. |
| 3488 | 23235923 | Access of corticotropin to glucocorticoid synthesis in adrenocortical cells is provided by the expression of the ACTH receptor (MC2R). |
| 3489 | 23235923 | Activation of the MC2R increases stimulatory G-protein, adenylyl cyclase, and protein kinase A (PKA) activities. |
| 3490 | 23235923 | Sensitivity of adrenocortical cells to renin/angiotensin-2 is conferred by the expression of the inhibitory G-protein-linked angiotensin-2 type 1 receptor (AT1R) that additionally associates to the phospholipase C-activating G-protein q. |
| 3491 | 23235923 | The AT1R is connected to the adrenal potassium sensory system and regulates calcium influx as well as phospholipase C-β (PLC-β) and thus calmodulin kinase-dependent transcription of steroidogenic enzymes. |
| 3492 | 23235923 | While AT1R signaling suppresses the influence of corticotropin on the generation of cyclic adenosine monophosphate, the expression of the AT1R and its associated enzyme activities are under the control of glucocorticoids. |
| 3493 | 23235923 | Control of CYP11B2/CYP11B1 expression ratio and consequences for the zonation of the adrenal cortex. |
| 3494 | 23235923 | Access of corticotropin to glucocorticoid synthesis in adrenocortical cells is provided by the expression of the ACTH receptor (MC2R). |
| 3495 | 23235923 | Activation of the MC2R increases stimulatory G-protein, adenylyl cyclase, and protein kinase A (PKA) activities. |
| 3496 | 23235923 | Sensitivity of adrenocortical cells to renin/angiotensin-2 is conferred by the expression of the inhibitory G-protein-linked angiotensin-2 type 1 receptor (AT1R) that additionally associates to the phospholipase C-activating G-protein q. |
| 3497 | 23235923 | The AT1R is connected to the adrenal potassium sensory system and regulates calcium influx as well as phospholipase C-β (PLC-β) and thus calmodulin kinase-dependent transcription of steroidogenic enzymes. |
| 3498 | 23235923 | While AT1R signaling suppresses the influence of corticotropin on the generation of cyclic adenosine monophosphate, the expression of the AT1R and its associated enzyme activities are under the control of glucocorticoids. |
| 3499 | 23386726 | Modulation of AgRP-neuronal function by SOCS3 as an initiating event in diet-induced hypothalamic leptin resistance. |
| 3500 | 23386726 | We show that agouti-related protein (AgRP)-expressing neurons precede proopiomelanocortin neurons in developing diet-induced cellular leptin resistance. |
| 3501 | 23386726 | High-fat diet-induced up-regulation of suppressor of cytokine signaling-3 (SOCS3) occurs in AgRP neurons before proopiomelanocortin and other hypothalamic neurons. |
| 3502 | 23386726 | SOCS3 expression in AgRP neurons increases after 2 d of high-fat feeding, but reduces after switching to a low-fat diet for 1 d. |
| 3503 | 23386726 | Consistently, transgenic overexpression of SOCS3 in AgRP neurons produces metabolic phenotypes resembling those observed after short-term high-fat feeding. |
| 3504 | 23386726 | AgRP neurons are more responsive to low levels of circulating leptin, but they are also more prone to development of leptin resistance in response to a small increase in blood leptin concentrations. |
| 3505 | 23386726 | Furthermore, modulation of SOCS3 expression in AgRP neurons may play a dynamic and physiological role in metabolic fine tuning in response to short-term changes of nutritional status. |
| 3506 | 23386726 | Modulation of AgRP-neuronal function by SOCS3 as an initiating event in diet-induced hypothalamic leptin resistance. |
| 3507 | 23386726 | We show that agouti-related protein (AgRP)-expressing neurons precede proopiomelanocortin neurons in developing diet-induced cellular leptin resistance. |
| 3508 | 23386726 | High-fat diet-induced up-regulation of suppressor of cytokine signaling-3 (SOCS3) occurs in AgRP neurons before proopiomelanocortin and other hypothalamic neurons. |
| 3509 | 23386726 | SOCS3 expression in AgRP neurons increases after 2 d of high-fat feeding, but reduces after switching to a low-fat diet for 1 d. |
| 3510 | 23386726 | Consistently, transgenic overexpression of SOCS3 in AgRP neurons produces metabolic phenotypes resembling those observed after short-term high-fat feeding. |
| 3511 | 23386726 | AgRP neurons are more responsive to low levels of circulating leptin, but they are also more prone to development of leptin resistance in response to a small increase in blood leptin concentrations. |
| 3512 | 23386726 | Furthermore, modulation of SOCS3 expression in AgRP neurons may play a dynamic and physiological role in metabolic fine tuning in response to short-term changes of nutritional status. |
| 3513 | 23425648 | Adrenocorticotropic hormone independent macronodular adrenal hyperplasia due to aberrant receptor expression: is medical treatment always an option? |
| 3514 | 23553410 | Routine haematology, serum biochemistry, urinalysis (including culture), total T4 and urine creatinine:cortisol ratio were unremarkable, but markedly increased insulin-like growth factor-1 concentration was identified and a pituitary mass was subsequently documented. |
| 3515 | 23553410 | A double-pituitary adenoma comprising a discrete somatotroph adenoma and a separate plurihormonal adenoma (positive immunoreactivity for ACTH, melanocyte-stimulating hormone and follicle-stimulating hormone) was identified on post-mortem examination. |
| 3516 | 23565411 | We report perhaps for the first time, TSH, GH, adrenocorticotrophic hormone (ACTH) and gonadotropins secreting pituitary macroadenoma diagnosed in a 40 year lady presenting with features of thyrotoxicosis for 5 months, amenorrhea for 3 months and newly diagnosed diabetes and hypertension for 2 months along with headache, nausea, and vomiting, who had acromegaloid habitus, grade-II goitre, increased uptake on Technitium-99 pertechnate thyroid scan (4.1%; normal: 0.24-3.34%), with increased T3 (5.98 pg/ ml; 1.5-4.1), increased T4 (2.34 ng/dl; 0.9-1.8), inappropriately high TSH (2.32 μIU/ml; 0.4-4.2), insulin like growth factor-1 (711 ng/ ml; 109-264), non-suppressed post-glucose GH (15.9 ng/ml; <1 ng/ml), normal estradiol (52 pg/ml; 21-251), inappropriately high luteinizing hormone (53.5 mIU/ml; 1.1-11.6), inappropriately high follicle stimulating hormone (59 mIU/ml; 3-14.4), non-suppressed overnight dexamethasone cortisol (5.8 mcg/dl; <2), elevated ACTH (58 pg/ml 5-15), withdrawal bleed on progestrogen challenge, bitemporal hemianopia on automated perimetry and pituitary macroadenoma on MRI imaging of sella. |
| 3517 | 23565490 | As a result of sustained leptin insufficiency, the hypothalamic restraint on pancreatic insulin secretion is lost. |
| 3518 | 23565490 | Additionally injection of rAVV-LEP into the hypothalamus suppressed the expression of orexigenic neuropeptide Y (NPY) and enhanced anorexigenic pro-opiomelanocortin (POMC) in the arcuate nucleus (ARC) in rats. |
| 3519 | 23590931 | The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress. |
| 3520 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3521 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3522 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3523 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3524 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3525 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3526 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3527 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3528 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3529 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3530 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3531 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3532 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3533 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3534 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3535 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3536 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3537 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3538 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3539 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3540 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3541 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3542 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3543 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3544 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3545 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3546 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3547 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3548 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3549 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3550 | 23640796 | Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. |
| 3551 | 23640796 | POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. |
| 3552 | 23640796 | Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. |
| 3553 | 23640796 | To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. |
| 3554 | 23640796 | In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. |
| 3555 | 23640796 | In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. |
| 3556 | 23649472 | The melanocortin system and insulin resistance in humans: insights from a patient with complete POMC deficiency and type 1 diabetes mellitus. |
| 3557 | 23730258 | We revisit the role of NPY and POMC neurons in the regulation of appetite and energy homeostasis, and consider how ROS and intracellular calcium levels affect these neurons. |
| 3558 | 23735822 | As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. |
| 3559 | 23735822 | Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. |
| 3560 | 23735822 | As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. |
| 3561 | 23735822 | Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. |
| 3562 | 23735822 | The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. |
| 3563 | 23735822 | Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. |
| 3564 | 23817596 | The aim of our study is to estimate the prevalence of MS (according to Cook's criteria) in a Chilean cross-sectional sample of 259 obese children (47.1% girls, aged 6-12 years), and to assess the association between common genetic variants of leptin-melanocortin pathway genes (LEP, LEPR, POMC, MC3R and MC4R) with components of the MS using logistic regression. |
| 3565 | 23835335 | Genetic ablation of FoxO1 in selected hypothalamic neurons decreases food intake, increases energy expenditure, and improves glucose homeostasis, highlighting the role of this gene in insulin and leptin signaling. |
| 3566 | 23835335 | Lineage-tracing experiments showed that NPY/AgRP and POMC neurons were minimally affected by the knockout. |
| 3567 | 23946678 | However, within several weeks, plasma ACTH returned to normal, and showed a normal increase response to corticotropin-releasing hormone stimulation test. |
| 3568 | 23979792 | QRFP, a member of the RFamide-related peptide family, is a strongly conserved hypothalamic neuropeptide that has been characterized in various species. |
| 3569 | 23979792 | Additionally, QRFP regulates the expression and release of hypothalamic Neuropeptide Y and proopiomelanocortin/α-Melanocyte-Stimulating Hormone. |
| 3570 | 24011066 | Leptin mimics many of the antidiabetic actions of insulin in insulin-deficient diabetes, but the mechanism is controversial. |
| 3571 | 24011066 | Fujikawa et al. (2013) reveal that leptin receptors in γ-aminobutyric acid (GABA)-ergic and pro-opiomelanocortin (POMC) neurons in the central nervous system are sufficient to mediate the lifesaving and antidiabetic actions of leptin in insulin-deficient mice. |