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Gene Information
Gene symbol: GNRH1
Gene name: gonadotropin-releasing hormone 1 (luteinizing-releasing hormone)
HGNC ID: 4419
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 351461 | [Behavior of blood testosterone, 17-beta-estradiol, LH and FSH after stimulation with HCG and LHRH in a group of diabetic subjects with sexual deficiency]. |
| 2 | 707005 | Primary empty sella syndrome with panhypopituitarism, diabetes insipidus, and visual field defects. |
| 3 | 707005 | Failure of growth hormone (hGH), cortisol and prolactin to respond to insulin induced hypoglycaemia (0.1 U/kg), of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to respond to gonadotrophin releasing hormone (GnRH, 100 microgram) and of thyrotrophin (TSH) and prolactin to increase after thyrotrophin releasing hormone (TRH, 500 microgram), confirmed the diagnosis of panhypopituitarism. |
| 4 | 1345561 | In each case plasma concentrations of LH, FSH, PRL, TSH, alpha-subunit, ACTH before and after appropriate stimulation with TRH, metoclopramid, LH-RH, GRF or metyrapon were determined with RIA. |
| 5 | 1752336 | For pituitary function tests, arginine infusion test, TRH, LH-RH or CRH test and insulin tolerance test were performed. |
| 6 | 1752336 | APA reacting to rat pituitary cytoplasmic antigens (pituitary cell antibodies: PCA) and APA reacting to rat GH3 cells and/or mouse AtT20 cells surface antigens (pituitary cell surface antibodies: PCSA) were assayed with indirect immunofluorescence method. |
| 7 | 1899217 | In vivo comparison of the follicle-stimulating hormone-suppressing activity of follistatin and inhibin in ovariectomized rats. |
| 8 | 1899217 | Data obtained from a second experiment conducted to examine the effects of inhibin and follistatin on anterior pituitary gonadotropin responses to LHRH were consistent with in vitro data showing direct pituitary effects of the gonadal polypeptides. |
| 9 | 2009995 | Luteinizing hormone (LH) responses to gonadotropin-releasing hormone (GnRH) (100 micrograms injected intravenously (IV)) or naloxone (4 mg injected plus 8 mg infused in 2 hours IV) were evaluated in 29 women with insulin-dependent diabetes mellitus (IDDM) (duration, group I (n = 15): less than 10 years, range 3 to 9 years; group II (n = 14): greater than 10 years, range 11 to 20 years) and in 15 normal controls, on the 22nd days of normal menstrual cycles. |
| 10 | 2111887 | All animals were sacrificed in either diestrus or proestrus for determination of GnRH concentration in the hypothalamus, LH and follicle-stimulating hormone (FSH) content in pituitary and LH, FSH, estradiol and corticosterone in serum. |
| 11 | 2111887 | GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals. |
| 12 | 2111887 | All animals were sacrificed in either diestrus or proestrus for determination of GnRH concentration in the hypothalamus, LH and follicle-stimulating hormone (FSH) content in pituitary and LH, FSH, estradiol and corticosterone in serum. |
| 13 | 2111887 | GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals. |
| 14 | 2116947 | Effects of improved blood glucose on insulin-induced hypoglycaemia, TRH, GnRH and exercise tests in insulin-dependent diabetes. |
| 15 | 2116947 | Growth hormone and cortisol response to hypoglycaemia and thyroid stimulating hormone and prolactin secretion in response to thyrotrophin releasing hormone were unaffected by residual beta-cell function or metabolic control. |
| 16 | 2492706 | Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression. |
| 17 | 2492706 | Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. |
| 18 | 2492706 | The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. |
| 19 | 2492706 | When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. |
| 20 | 2492706 | These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression. |
| 21 | 2492706 | Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression. |
| 22 | 2492706 | Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. |
| 23 | 2492706 | The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. |
| 24 | 2492706 | When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. |
| 25 | 2492706 | These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression. |
| 26 | 2492706 | Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression. |
| 27 | 2492706 | Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. |
| 28 | 2492706 | The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. |
| 29 | 2492706 | When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. |
| 30 | 2492706 | These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression. |
| 31 | 2492706 | Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression. |
| 32 | 2492706 | Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. |
| 33 | 2492706 | The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. |
| 34 | 2492706 | When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. |
| 35 | 2492706 | These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression. |
| 36 | 2492706 | Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression. |
| 37 | 2492706 | Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. |
| 38 | 2492706 | The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. |
| 39 | 2492706 | When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. |
| 40 | 2492706 | These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression. |
| 41 | 2507379 | Thus, several pathogenetic mechanisms might be involved in reduced gonadotropin and TSH release at the cellular level: 1) anatomical lesions of organelles involved in glycoprotein hormone synthesis and secretion, possibly due to insulin deficiency; 2) decreased gonadotropin-releasing hormone (GnRH) and thyrotropin-releasing hormone (TRH) receptors on pituitary cells; 3) inadequate GnRH and TRH stimulation; 4) high plasma corticosterone levels; or 5) a combination of points 1-4. |
| 42 | 2781979 | An abnormal growth hormone (GH) increase after non-specific stimuli (such as TRH, LHRH and, in a few cases, metoclopramide), has been described in insulin-dependent diabetes. |
| 43 | 2811647 | In several patients stimulation test with specific releasing factors (TRH, LHRH, oCRH) were carried out. |
| 44 | 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. |
| 45 | 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. |
| 46 | 3059985 | In diabetic men, the hypothalamic-hypophyseal-gonadal axis seems to be normal (with exception of individual cases); Mean plasma levels of testosterone, LH, FSH and the responses of the gonadal axis to hCG and LHRH are normal. |
| 47 | 3138279 | The patients with small pituitary glands had delayed or prolonged serum TSH responses to TRH and impaired serum LH and FSH responses to GnRH; 4 of the patients with normal-sized pituitary glands had normal serum TSH, LH, and FSH responses. |
| 48 | 3332566 | The effect of improving diabetic control on secondary hypogonadotropic amenorrhea was investigated in patients with insulin-dependent diabetes mellitus (IDDM). |
| 49 | 3332566 | After six months of improved metabolic control (n = 5) using intensified conventional therapy or continuous subcutaneous insulin infusion, the level of glycosylated hemoglobin dropped from 11.8 +/- 0.9 percent to 8.5 +/- 0.5 percent (p less than 0.005), and body weight increased from 60.5 +/- 1.8 kg to 64.7 +/- 1.4 kg (p less than 0.02). |
| 50 | 3332566 | There was no significant change in serum levels of estradiol, progesterone, dihydroxyepiandrosterone, testosterone, prolactin, basal or GnRH-stimulated luteinizing hormone, or follicle-stimulating hormone. |
| 51 | 3924695 | Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. |
| 52 | 3924695 | Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. |
| 53 | 3924695 | There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. |
| 54 | 3924695 | Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. |
| 55 | 3924695 | Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. |
| 56 | 3924695 | There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. |
| 57 | 4347096 | The response to TRH, LH-RH, metyrapone and vasopressin in patients with hypothalamo-pituitary disorders. |
| 58 | 6403566 | Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. |
| 59 | 6403566 | Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. |
| 60 | 6403566 | The FSH response to GnRH and the PRL response to TRH were similar in all groups. |
| 61 | 6403566 | It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. |
| 62 | 6403566 | Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. |
| 63 | 6403566 | Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. |
| 64 | 6403566 | The FSH response to GnRH and the PRL response to TRH were similar in all groups. |
| 65 | 6403566 | It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. |
| 66 | 6403566 | Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. |
| 67 | 6403566 | Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. |
| 68 | 6403566 | The FSH response to GnRH and the PRL response to TRH were similar in all groups. |
| 69 | 6403566 | It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. |
| 70 | 6780440 | The hormonal response to LHRH and TRH was evaluated in three groups of male diaetics. |
| 71 | 6820063 | Endocrine challenge tests with GnRH and TRH before and after stalk transection indicated a loss of responsiveness (GnRH) or suppressed responsiveness (TRH) after the operation. |
| 72 | 6987324 | Chromatography of an extract of SME from 20 DIhomo rats on BioGel P2 resulted in a loss of CRF activity and the emergence of two regions of CRF activity: the peak at the void volume of the column and the later eluting peak which also had some LH-RH bioactivity but no immunoactivity. |
| 73 | 6987324 | When synthetic arginine-vasopressin was added to Brattleboro SME in amounts equivalent to those found in normal SME the CRF bioactivity was dramatically potentiated. |
| 74 | 7019531 | The patient had also experienced secondary amenorrhea with sub-normal follicle-stimulating-hormone (FSH) and luteinizing hormone (LH) levels, both of which demonstrated a prolonged sluggish response to an injection of gonadotropin-releasing hormone (GnRH); this response suggested hypogonadotropic hypogonadism, possibly on the basis of a tumor involving both pituitary and hypothalamus. |
| 75 | 7554320 | Chromosomal analysis with trypsin banding was normal and biochemical evaluation revealed low oestrogen levels, inappropriately low gonadotrophins, very low IGF-I concentrations and GH concentrations unresponsive to insulin or L-dopa administration. |
| 76 | 7554320 | Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. |
| 77 | 7554320 | The presence of congenital combined growth hormone and gonadotrophin deficiency on the basis of a suprapituitary defect suggests the existence of common or related pathways regulating GnRH and GHRH synthesis or secretion and may have contributed to the ultimate development of insulin resistance and hyperlipidaemia. |
| 78 | 7554320 | Chromosomal analysis with trypsin banding was normal and biochemical evaluation revealed low oestrogen levels, inappropriately low gonadotrophins, very low IGF-I concentrations and GH concentrations unresponsive to insulin or L-dopa administration. |
| 79 | 7554320 | Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. |
| 80 | 7554320 | The presence of congenital combined growth hormone and gonadotrophin deficiency on the basis of a suprapituitary defect suggests the existence of common or related pathways regulating GnRH and GHRH synthesis or secretion and may have contributed to the ultimate development of insulin resistance and hyperlipidaemia. |
| 81 | 7591703 | Exaggerated growth hormone (GH) responses to various provocative stimuli have been reported previously in insulin-dependent diabetes mellitus (IDDM). |
| 82 | 7591703 | We investigated GH, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels after GnRH administration in seven IDDM and eight non-insulin-dependent diabetic (NIDDM) patients. |
| 83 | 7591703 | These results suggest that poorly controlled IDDM and NIDDM does not lead to inappropriate GH responses to GnRH. |
| 84 | 7591703 | Exaggerated growth hormone (GH) responses to various provocative stimuli have been reported previously in insulin-dependent diabetes mellitus (IDDM). |
| 85 | 7591703 | We investigated GH, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels after GnRH administration in seven IDDM and eight non-insulin-dependent diabetic (NIDDM) patients. |
| 86 | 7591703 | These results suggest that poorly controlled IDDM and NIDDM does not lead to inappropriate GH responses to GnRH. |
| 87 | 7664670 | To elucidate the roles of the hypothalamic peptides, GH-releasing hormone (GRH) and somatostatin (SRIH), potentially responsible for altered GH dynamics in diabetes, we studied the time courses of their changes in level associated with altered GH secretion in streptozotocin (STZ)-induced diabetic mice. |
| 88 | 7674023 | Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. |
| 89 | 7674023 | The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone-releasing hormone (GRH)-produced pancreatic tumor is reported. |
| 90 | 7826593 | Disordered reproductive function has long been recognized as a prevalent problem among women of reproductive age who suffer from insulin-dependent diabetes mellitus (IDDM). |
| 91 | 7826593 | Similarly, pituitary function as assessed by basal gonadotrophins and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release appears to be normal in young women with IDDM. |
| 92 | 7826593 | It appears that the oligo/amenorrhea noted in IDDM is principally hypothalamic in origin and may represent intermittent (and perhaps reversible) failure of the GnRH pulse generator, similar to the situation observed in women who engage in endurance training or who suffer from anorexia nervosa. |
| 93 | 7826593 | Disordered reproductive function has long been recognized as a prevalent problem among women of reproductive age who suffer from insulin-dependent diabetes mellitus (IDDM). |
| 94 | 7826593 | Similarly, pituitary function as assessed by basal gonadotrophins and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release appears to be normal in young women with IDDM. |
| 95 | 7826593 | It appears that the oligo/amenorrhea noted in IDDM is principally hypothalamic in origin and may represent intermittent (and perhaps reversible) failure of the GnRH pulse generator, similar to the situation observed in women who engage in endurance training or who suffer from anorexia nervosa. |
| 96 | 8045738 | GH and GHBP activity and not IGF-1 and its receptor activity express growth velocity reduction during treatment of central precocious puberty by a superactive GNRH analogue. |
| 97 | 8201916 | Basal hormone levels were normal for thyroxin, thyrotropin, FSH, LH, prolactin, hGH and cortisol; the responses to pituitary stimulation with TRH and LHRH were subnormal or nil. |
| 98 | 8254951 | A combination of CRF, GRF, TRH and GnRH is a safer and more reliable test to evaluate pituitary function than the conventional triple test consisting of insulin, TRH and GnRH, especially in patients predicted to have pituitary-adrenal insufficiency. |
| 99 | 8333840 | Differential control of activin, inhibin and follistatin proteins in cultured rat granulosa cells. |
| 100 | 8333840 | Follistatin, activin and inhibin proteins are produced by granulosa cells, but the mechanisms controlling their production remain unclear. |
| 101 | 8333840 | Here, we examined how the protein kinase A (PKA) and protein kinase C (PKC) pathways act and interact to regulate production of these proteins. |
| 102 | 8333840 | Conditioned media were assayed for inhibin and activin by ligand blotting using recombinant human 125I-follistatin and for follistatin by double ligand blotting using cold activin plus 125I-follistatin. |
| 103 | 8333840 | In contrast, GnRH and TPA stimulated activin, and to a lesser degree, inhibin production; significantly, this is the first demonstration of activin dimer production by granulosa cells. |
| 104 | 8473380 | To investigate hypothalamic and/or pituitary abnormalities in women with poorly controlled insulin-dependent diabetes mellitus (IDDM) and secondary amenorrhea, we measured serum LH every 10 min for 24 h and for 2 additional h after the administration of exogenous GnRH in 8 women with IDDM and amenorrhea and compared these to data from 15 eumenorrheic nondiabetic women. |
| 105 | 8473380 | The IDDM women responded to a 10-micrograms GnRH bolus with LH pulses of larger total (51 +/- 15.9 vs. 15 +/- 1.4 IU/L; P < 0.01) and incremental (29 +/- 7.6 vs. 9 +/- 1.2; P < 0.001) amplitude. |
| 106 | 8473380 | To investigate hypothalamic and/or pituitary abnormalities in women with poorly controlled insulin-dependent diabetes mellitus (IDDM) and secondary amenorrhea, we measured serum LH every 10 min for 24 h and for 2 additional h after the administration of exogenous GnRH in 8 women with IDDM and amenorrhea and compared these to data from 15 eumenorrheic nondiabetic women. |
| 107 | 8473380 | The IDDM women responded to a 10-micrograms GnRH bolus with LH pulses of larger total (51 +/- 15.9 vs. 15 +/- 1.4 IU/L; P < 0.01) and incremental (29 +/- 7.6 vs. 9 +/- 1.2; P < 0.001) amplitude. |
| 108 | 8796342 | Three months after the head injury, the hormonal evaluation of the hypothalamic-pituitary axis by means of insulin stress test with the simultaneous administration of TRH and GnRH resulted in reduced responses of GH, cortisol, TSH, FSH, and LH with low baseline serum concentrations of free T4 and testosterone. |
| 109 | 8817243 | Two tumours did not respond to PACAP, although LHRH was stimulatory in these. |
| 110 | 8817243 | These results indicate that PACAP can directly stimulate LH and FSH secretion by human pituitary gonadotrophs and that PACAP-receptors in gonadotrophin-secreting tumours are coupled with adenylate cyclase but not the PI second messenger system. |
| 111 | 8957739 | TRH and LHRH tests were not systematically performed. |
| 112 | 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. |
| 113 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 114 | 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. |
| 115 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 116 | 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. |
| 117 | 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. |
| 118 | 9228515 | CRF induced a rise in extracellular concentration of NA and 5-HT only in the estrous ewes prior to a preovulatory LH surge. |
| 119 | 9228515 | CRF treatment caused a heterogenous effect on extra-cellular concentrations of 5-HT in ewes during the preovulatory LH surge. |
| 120 | 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. |
| 121 | 9245068 | Is leptin and insulin resistance in the X-5H hormonal metabolic syndrome a parallel or causally-linked phenomenon?]. |
| 122 | 9245068 | It seems that leptin controls not only the function of the hypothalamic satiety centre but also the output of GnRh and other liberins as well as thermoregulation, muscular and sexual activity and thus energy expenditure. |
| 123 | 9245068 | In the insulin resistance syndrome (5H-X) it may thus be assumed that there is a parallel leptin and insulin resistance, probably of the postreceptor type, and even a causal association, as the "db" gene is identical with the gene for leptin receptors. |
| 124 | 9264049 | LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats. |
| 125 | 9264049 | Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells. |
| 126 | 9264049 | To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats. |
| 127 | 9264049 | The number of LHRH receptor-bearing cells in diabetic animals was increased. |
| 128 | 9264049 | We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland. |
| 129 | 9264049 | LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats. |
| 130 | 9264049 | Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells. |
| 131 | 9264049 | To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats. |
| 132 | 9264049 | The number of LHRH receptor-bearing cells in diabetic animals was increased. |
| 133 | 9264049 | We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland. |
| 134 | 9264049 | LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats. |
| 135 | 9264049 | Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells. |
| 136 | 9264049 | To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats. |
| 137 | 9264049 | The number of LHRH receptor-bearing cells in diabetic animals was increased. |
| 138 | 9264049 | We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland. |
| 139 | 9264049 | LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats. |
| 140 | 9264049 | Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells. |
| 141 | 9264049 | To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats. |
| 142 | 9264049 | The number of LHRH receptor-bearing cells in diabetic animals was increased. |
| 143 | 9264049 | We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland. |
| 144 | 9264049 | LHRH receptors and LHRH receptor-bearing cells in pituitaries of streptozocin diabetic male rats. |
| 145 | 9264049 | Possible causes for the gonadotrope disorders may be low hypothalamic LHRH secretion alone or combined with reduced (a) number of LHRH receptor sites, or (b) receptor to ligand affinity, or (c) of LHRH receptor-bearing cells. |
| 146 | 9264049 | To clarify this question we determined by saturation and competition binding Bmax, KD and KA of the LHRH receptor sites and counted the receptor-bearing cells in pituitary glands of control and STZ-diabetic adult male rats. |
| 147 | 9264049 | The number of LHRH receptor-bearing cells in diabetic animals was increased. |
| 148 | 9264049 | We conclude that the reduced LH secretion from the diabetic pituitary gland might be due to a reduced number of LHRH receptor sites in the pituitary gland. |
| 149 | 9439932 | Involvement of gamma amino butyric acid (GABA) in the postnatal function of the GnRH pulse generator as determined on the basis of GnRH and GnRH-receptor gene expression in the hypothalamus and the pituitary. |
| 150 | 9447286 | Prior to adrenalectomy, TSH, GH or LH showed a low response to TRH, GHRH or LHRH, respectively. |
| 151 | 9481560 | Changes in serum glucose levels were examined in a female with insulin-independent diabetes who received a gonadotropin-releasing hormone (GnRH) analog treatment for pelvic endometriosis. |
| 152 | 9675568 | Ovulation induction with pulsatile GnRH in a patient with anovulation of hypothalamic origin and central diabetes insipidus. |
| 153 | 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. |
| 154 | 10077358 | In all subjects under GnRH antagonist treatment a marked suppression of LH, FSH, testosterone, DHT and estradiol was observed. |
| 155 | 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). |
| 156 | 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. |
| 157 | 10099967 | The responses of pituitary gonadotrophins to GnRH, and of thyroid stimulating hormone (TSH) to TRH, were similar in both groups. |
| 158 | 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. |
| 159 | 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). |
| 160 | 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. |
| 161 | 10099967 | The responses of pituitary gonadotrophins to GnRH, and of thyroid stimulating hormone (TSH) to TRH, were similar in both groups. |
| 162 | 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. |
| 163 | 10775173 | These findings support the contention that insulin and/or insulin-dependent changes in glucose availability modulate LH(GnRH) pulse frequency, and that such effects are potentiated by, but not dependent upon, gonadal steroids. |
| 164 | 10775174 | These results are consistent with the notion that central insulin plays a role in regulating pulsatile GnRH secretion. |
| 165 | 11036877 | Pituitary apoplexy has been reported as a very rare complication of combined tests of anterior pituitary function and of TRH or gonadotropin-releasing hormone (GnRH) administration in pituitary tumor. |
| 166 | 11036877 | A 34-year-old man with a GH-secreting pituitary macroadenoma and diabetes mellitus received an injection of 400 microg TRH, 100 microg GnRH, and 0.15 U/Kg regular insulin. |
| 167 | 11036877 | Postoperative course was uneventful and his serum insulin-like growth factor-1 (IGF-1) level and blood glucose levels were normalized. |
| 168 | 11036877 | Pituitary apoplexy has been reported as a very rare complication of combined tests of anterior pituitary function and of TRH or gonadotropin-releasing hormone (GnRH) administration in pituitary tumor. |
| 169 | 11036877 | A 34-year-old man with a GH-secreting pituitary macroadenoma and diabetes mellitus received an injection of 400 microg TRH, 100 microg GnRH, and 0.15 U/Kg regular insulin. |
| 170 | 11036877 | Postoperative course was uneventful and his serum insulin-like growth factor-1 (IGF-1) level and blood glucose levels were normalized. |
| 171 | 11125008 | Gonadotropin-releasing hormone (GnRH) secretion from native and immortalized hypothalamic neurons is regulated by endogenous Ca(2+)-mobilizing and adenylyl cyclase (AC)-coupled receptors. |
| 172 | 11193441 | The plasma concentrations of GH, TSH, LH, FSH, ACTH and ADH were low or below the detectable limits. |
| 173 | 11193441 | Arginine, LH-RH, TRH and CRH tolerance tests revealed no or low responses of GH, LH/FSH, TSH, and ACTH/cortisol, respectively. |
| 174 | 11453030 | Serotonin (5-HT), GABA and catecholamines (CA) have qualitative differences in the effects on GnRH and LH secretion in early prepubertal than in late prepubertal and adult female rats. |
| 175 | 11453030 | The administration of 5-hydroxytryptophan a precursor of serotonin (5-HT) which increases 5-HT hypothalamic levels induces GnRH and LH release in early prepubertal female rats, these effects dissapear in late prepubertal stage having an inhibitory action in adult female rats. |
| 176 | 11453030 | Serotonin (5-HT), GABA and catecholamines (CA) have qualitative differences in the effects on GnRH and LH secretion in early prepubertal than in late prepubertal and adult female rats. |
| 177 | 11453030 | The administration of 5-hydroxytryptophan a precursor of serotonin (5-HT) which increases 5-HT hypothalamic levels induces GnRH and LH release in early prepubertal female rats, these effects dissapear in late prepubertal stage having an inhibitory action in adult female rats. |
| 178 | 11826765 | Ovulation induction with pulsatile gonadotropin-releasing hormone (GnRH) or gonadotropins in a case of hypothalamic amenorrhea and diabetes insipidus. |
| 179 | 11826765 | Cortisol and prolactin responded normally to a combined insulin tolerance test (ITT) and thyrotropin-releasing hormone (TRH) challenge, while thyroid-stimulating hormone (TSH) response to TRH was diminished, and no response of growth hormone to ITT was detected. |
| 180 | 11826765 | Both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels increased following gonadotropin-releasing hormone (GnRH) challenge. |
| 181 | 11826765 | Ovulation induction with pulsatile gonadotropin-releasing hormone (GnRH) or gonadotropins in a case of hypothalamic amenorrhea and diabetes insipidus. |
| 182 | 11826765 | Cortisol and prolactin responded normally to a combined insulin tolerance test (ITT) and thyrotropin-releasing hormone (TRH) challenge, while thyroid-stimulating hormone (TSH) response to TRH was diminished, and no response of growth hormone to ITT was detected. |
| 183 | 11826765 | Both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels increased following gonadotropin-releasing hormone (GnRH) challenge. |
| 184 | 11868239 | The anterior pituitary insufficiency was defined as an inadequate excretory response to metopirone, LH-RH and TRH stimulation. |
| 185 | 12107209 | Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. |
| 186 | 12107209 | The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. |
| 187 | 12107209 | The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. |
| 188 | 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). |
| 189 | 12107209 | The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. |
| 190 | 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. |
| 191 | 12107209 | Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. |
| 192 | 12107209 | The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. |
| 193 | 12107209 | The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. |
| 194 | 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). |
| 195 | 12107209 | The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. |
| 196 | 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. |
| 197 | 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. |
| 198 | 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. |
| 199 | 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. |
| 200 | 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. |
| 201 | 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. |
| 202 | 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. |
| 203 | 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. |
| 204 | 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. |
| 205 | 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. |
| 206 | 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. |
| 207 | 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. |
| 208 | 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. |
| 209 | 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. |
| 210 | 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. |
| 211 | 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. |
| 212 | 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. |
| 213 | 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. |
| 214 | 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. |
| 215 | 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. |
| 216 | 12466346 | To more clearly define the impact of early diabetic alterations in the male reproductive axis, we applied a combined strategy of patient selection restricted to young men with relatively short duration of IDDM, dual control groups, multiparameter deconvolution analysis to assess LH secretory activity, and assessment of time-dependent changes in human chorionic gonadotropin (hCG)-stimulated serum testosterone concentrations. |
| 217 | 12466346 | Uncontrolled IDDM patients had significantly (P < 0.05) lower integrated serum LH concentrations after the first and second GnRH pulses (first GnRH pulse, 4460 +/- 770 vs. 7250 +/- 1200 and 5120 +/- 910 IU/liter; second pulse, 4700 +/- 615 vs. 7640 +/- 881 and 7100 +/- 1230 IU/liter; poorly controlled vs. well controlled IDDM and healthy men, respectively) and markedly attenuated LH secretory burst mass after the second GnRH stimulus (49 +/- 8.8 vs. 90 +/- 13 and 83 +/- 19 IU/liter; poorly controlled vs. well controlled IDDM and healthy controls, respectively). |
| 218 | 12466346 | The biological to immunological ratio of LH released in baseline conditions was higher in uncontrolled IDDM patients (0.81 +/- 0.10) than in controlled IDDM (0.37 +/- 0.08) and healthy controls (0.48 +/- 0.06; P < 0.01), whereas LH released in response to exogenous GnRH exhibited comparable ratios among the three study cohorts. |
| 219 | 12466346 | Collectively, these results indicate that the function of the hypothalamic-gonadotrope axis is compromised in young men with poorly controlled IDDM, such that the amplitude of spontaneous pulsatile and exogenous GnRH-stimulated LH secretion is attenuated. |
| 220 | 12466346 | To more clearly define the impact of early diabetic alterations in the male reproductive axis, we applied a combined strategy of patient selection restricted to young men with relatively short duration of IDDM, dual control groups, multiparameter deconvolution analysis to assess LH secretory activity, and assessment of time-dependent changes in human chorionic gonadotropin (hCG)-stimulated serum testosterone concentrations. |
| 221 | 12466346 | Uncontrolled IDDM patients had significantly (P < 0.05) lower integrated serum LH concentrations after the first and second GnRH pulses (first GnRH pulse, 4460 +/- 770 vs. 7250 +/- 1200 and 5120 +/- 910 IU/liter; second pulse, 4700 +/- 615 vs. 7640 +/- 881 and 7100 +/- 1230 IU/liter; poorly controlled vs. well controlled IDDM and healthy men, respectively) and markedly attenuated LH secretory burst mass after the second GnRH stimulus (49 +/- 8.8 vs. 90 +/- 13 and 83 +/- 19 IU/liter; poorly controlled vs. well controlled IDDM and healthy controls, respectively). |
| 222 | 12466346 | The biological to immunological ratio of LH released in baseline conditions was higher in uncontrolled IDDM patients (0.81 +/- 0.10) than in controlled IDDM (0.37 +/- 0.08) and healthy controls (0.48 +/- 0.06; P < 0.01), whereas LH released in response to exogenous GnRH exhibited comparable ratios among the three study cohorts. |
| 223 | 12466346 | Collectively, these results indicate that the function of the hypothalamic-gonadotrope axis is compromised in young men with poorly controlled IDDM, such that the amplitude of spontaneous pulsatile and exogenous GnRH-stimulated LH secretion is attenuated. |
| 224 | 12466346 | To more clearly define the impact of early diabetic alterations in the male reproductive axis, we applied a combined strategy of patient selection restricted to young men with relatively short duration of IDDM, dual control groups, multiparameter deconvolution analysis to assess LH secretory activity, and assessment of time-dependent changes in human chorionic gonadotropin (hCG)-stimulated serum testosterone concentrations. |
| 225 | 12466346 | Uncontrolled IDDM patients had significantly (P < 0.05) lower integrated serum LH concentrations after the first and second GnRH pulses (first GnRH pulse, 4460 +/- 770 vs. 7250 +/- 1200 and 5120 +/- 910 IU/liter; second pulse, 4700 +/- 615 vs. 7640 +/- 881 and 7100 +/- 1230 IU/liter; poorly controlled vs. well controlled IDDM and healthy men, respectively) and markedly attenuated LH secretory burst mass after the second GnRH stimulus (49 +/- 8.8 vs. 90 +/- 13 and 83 +/- 19 IU/liter; poorly controlled vs. well controlled IDDM and healthy controls, respectively). |
| 226 | 12466346 | The biological to immunological ratio of LH released in baseline conditions was higher in uncontrolled IDDM patients (0.81 +/- 0.10) than in controlled IDDM (0.37 +/- 0.08) and healthy controls (0.48 +/- 0.06; P < 0.01), whereas LH released in response to exogenous GnRH exhibited comparable ratios among the three study cohorts. |
| 227 | 12466346 | Collectively, these results indicate that the function of the hypothalamic-gonadotrope axis is compromised in young men with poorly controlled IDDM, such that the amplitude of spontaneous pulsatile and exogenous GnRH-stimulated LH secretion is attenuated. |
| 228 | 12535152 | These results suggest that ER beta is involved in the suppression of GnRH mRNA expression by coumestrol. |
| 229 | 12566943 | We assessed the activity and number of hypothalamic gonadotropin-releasing hormone (GnRH) neurons by double label immunocytochemistry for C-FOS and GnRH to determine if decreased GnRH neuron activity or number could account for the diabetes-induced deficits in neuroendocrine function. |
| 230 | 12674849 | Patients underwent dynamic endocrine testing consisting of insulin-induced hypoglycemia and anterior pituitary stimulation tests GnRH and TRH. |
| 231 | 12861226 | Leptin accelerates gonadotropin-releasing hormone (GnRH) pulsatility in hypothalamic neurons, and it has a direct effect on the anterior pituitary. |
| 232 | 12878721 | We show that both LbetaT2 cells and adult rat pituitaries express MIS type II receptor (MISRII) mRNA. |
| 233 | 12878721 | Within 2 h, follicle-stimulating hormone beta subunit (FSHbeta) mRNA levels are significantly induced by addition of MIS to LbetaT2 cells and remain elevated through 8 h of treatment. |
| 234 | 12878721 | Transcriptional activation of both the FSHbeta and luteinizing hormone beta subunit (LHbeta) gene promoters was observed by MIS, which enhances the effect of gonadotropin-releasing hormone (GnRH) agonist on the FSHbeta gene promoter and synergizes with the GnRH agonist to stimulate LHbeta gene promoter activity. |
| 235 | 12878721 | Addition of MIS to LbetaT2 cells stimulates the activity of the rat LHbeta gene promoter with as little as 1 microg/ml and in a dose-dependent manner. |
| 236 | 12878721 | These studies report both MISRII expression in rat pituitary cells and a gonadotrope-derived cell line and MIS-mediated activation of LHbeta and FSHbeta gene expression, and suggest that MIS may modulate the hypothalamic-pituitary-gonadal axis at more than one level. |
| 237 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 238 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 239 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 240 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 241 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 242 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 243 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 244 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 245 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 246 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 247 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 248 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 249 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 250 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 251 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 252 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 253 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 254 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 255 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 256 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 257 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 258 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 259 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 260 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 261 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 262 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 263 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 264 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 265 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 266 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 267 | 12951633 | Effect of leptin on hypothalamic release of GnRH and neurotransmitter amino acids during sexual maturation in female rats. |
| 268 | 12951633 | The purpose of the present study was to analyse the effect of leptin treatment on the hypothalamic release of GnRH, GABA, and the excitatory amino acids (EAA), aspartate (ASP) and glutamate (GLU) involved in NMDA neurotransmission in prepubertal (15 day old) and peripubertal (30 day old) female rats. |
| 269 | 12951633 | The hypothalamic release of GnRH was increased by leptin at both ages, the release being significantly higher in peripubertal than in prepubertal rats. |
| 270 | 12951633 | In conclusion, the results showed that leptin increased GnRH release by the hypothalamus of prepubertal and peripubertal rats. |
| 271 | 12951633 | These results and previous reports suggest that at this stage of sexual maturation, leptin exerts an stimulatory effect on GnRH by inducing release of excitatory amino acids (ASP) and reducing release of inhibitory amino acids (GABA) involved in GnRH control. |
| 272 | 12951633 | In prepubertal rats the stimulating effect of the adipocyte hormone on GnRH appears to be related to its stimulative action on GABA which at this age increases GnRH release. |
| 273 | 12959992 | To test whether the increased incidence of diabetes in castrated male NOD mice is related to an increase in GnRH activity, we treated castrated male NOD mice with Antide, a GnRH receptor antagonist, to determine the effect on the incidence and timing of onset of diabetes. |
| 274 | 14715715 | Although the infertility of Cpe(fat/fat) mice has not been systematically investigated, it is thought to be due to a deficit in GnRH processing. |
| 275 | 14736738 | Although the site of action of CGRP remains to be established, the induction of c-Fos expression in the preoptic area and hypothalamic paraventricular nucleus might suggest an involvement of these brain regions. |
| 276 | 14736738 | Coadministration (intracerebroventricular) of CGRP (400 pmol) with a CRH antagonist (alpha-helical CRF(9-41), 26 nmol) partly blocked the CGRP-induced suppression of LH pulses. |
| 277 | 14736738 | These results suggest that the suppression of pulsatile LH secretion by central administration of CGRP may be mediated in part by CRH, and that CGRP may play a pivotal role in the normal physiological response of stress-induced suppression of the hypothalamic GnRH pulse generator, and hence the reproductive system. |
| 278 | 14751362 | Combination of LHRH analog with somatostatin analog and dexamethasone versus chemotherapy in hormone-refractory prostate cancer: a randomized phase II study. |
| 279 | 15127327 | A few-day shift of the preovulatory GnRH/LH surge, as determined by estrous behavior, might, however, be a consequence of the PRL-induced increase in catecholamine turnover in the IN/ME. |
| 280 | 15232060 | The FSH-beta and GnRH-receptor genes are up-regulated by pituitary activin and down-regulated by pituitary follistatin, and circulating inhibin disrupts this local regulation by functioning as an endogenous competitor of the activin receptor. |
| 281 | 15232060 | There is evidence that the intra-pituitary regulation of FSH-beta and GnRH-receptor gene expression may activate pubertal maturation in male rats. |
| 282 | 15232060 | The FSH-beta and GnRH-receptor genes are up-regulated by pituitary activin and down-regulated by pituitary follistatin, and circulating inhibin disrupts this local regulation by functioning as an endogenous competitor of the activin receptor. |
| 283 | 15232060 | There is evidence that the intra-pituitary regulation of FSH-beta and GnRH-receptor gene expression may activate pubertal maturation in male rats. |
| 284 | 15319828 | Inhibin, activin, and follistatin were first identified as gonadal hormones that could exert selective effects on follicle-stimulating hormone (FSH) secretion without affecting luteinizing hormone (LH). |
| 285 | 15319828 | Although the primary source of inhibin remains the gonad, both activin and follistatin are produced in extragonadal tissues and can exert effects on FSH through an autocrine-paracrine mechanism. |
| 286 | 15319828 | Second, activin up-regulates gonadotropin-releasing hormone receptor (GnRHR) gene expression, leading to alterations in the synthesis and release of both gonadotropins in response to GnRH. |
| 287 | 15319828 | Third, activin can stimulate GnRH release from GnRH neurons in the hypothalamus and thereby affect FSH and LH secretion. |
| 288 | 15319828 | Both inhibin and follistatin can negatively regulate these effects by preventing activin binding to the activin receptor at the cell membrane and blocking activation of downstream signal transduction pathways. |
| 289 | 15319828 | This review concentrates on the mechanisms through which inhibin, activin, and follistatin regulate the gonadotropins. |
| 290 | 15319828 | The mechanisms of inhibin and activin signaling are also reported, with particular attention to developments in our understanding of inhibin receptor action and activin-induced transcriptional regulation of the FSHbeta gene promoter. |
| 291 | 15319828 | Inhibin, activin, and follistatin were first identified as gonadal hormones that could exert selective effects on follicle-stimulating hormone (FSH) secretion without affecting luteinizing hormone (LH). |
| 292 | 15319828 | Although the primary source of inhibin remains the gonad, both activin and follistatin are produced in extragonadal tissues and can exert effects on FSH through an autocrine-paracrine mechanism. |
| 293 | 15319828 | Second, activin up-regulates gonadotropin-releasing hormone receptor (GnRHR) gene expression, leading to alterations in the synthesis and release of both gonadotropins in response to GnRH. |
| 294 | 15319828 | Third, activin can stimulate GnRH release from GnRH neurons in the hypothalamus and thereby affect FSH and LH secretion. |
| 295 | 15319828 | Both inhibin and follistatin can negatively regulate these effects by preventing activin binding to the activin receptor at the cell membrane and blocking activation of downstream signal transduction pathways. |
| 296 | 15319828 | This review concentrates on the mechanisms through which inhibin, activin, and follistatin regulate the gonadotropins. |
| 297 | 15319828 | The mechanisms of inhibin and activin signaling are also reported, with particular attention to developments in our understanding of inhibin receptor action and activin-induced transcriptional regulation of the FSHbeta gene promoter. |
| 298 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 299 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 300 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 301 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 302 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 303 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 304 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 305 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 306 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 307 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 308 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 309 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 310 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 311 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 312 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 313 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 314 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 315 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 316 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 317 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 318 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 319 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 320 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 321 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 322 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 323 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 324 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 325 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 326 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 327 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 328 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 329 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 330 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 331 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 332 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 333 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 334 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 335 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 336 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 337 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 338 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 339 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 340 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 341 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 342 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 343 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 344 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 345 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 346 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 347 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 348 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 349 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 350 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 351 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 352 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 353 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 354 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 355 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 356 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 357 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 358 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 359 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 360 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 361 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 362 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 363 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 364 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 365 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 366 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 367 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 368 | 15375186 | Synergy between activin A and gonadotropin-releasing hormone in transcriptional activation of the rat follicle-stimulating hormone-beta gene. |
| 369 | 15375186 | Both activin and GnRH can independently stimulate expression of the FSHbeta subunit gene. |
| 370 | 15375186 | In this study, we used the gonadotrope-derived LbetaT2 cell line to investigate the potential interaction between activin and GnRH in regulating the transcriptional activity of the rat FSHbeta gene promoter. |
| 371 | 15375186 | Activin A and GnRH synergistically enhanced rat FSHbeta transcriptional activity. |
| 372 | 15375186 | Overexpression of SMAD3 (mediator of decapentaplegic-related protein 3), but not of SMAD2, increased transcriptional activation of the rat (r) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 (3+4). |
| 373 | 15375186 | The stimulatory effects of SMAD3 overexpression were localized to -472/-256 of the rFSHbeta gene promoter, and activin- and GnRH-responsive proteins were shown to bind to region -284/-252. |
| 374 | 15375186 | Mutation of two bases located in the center of this palindrome effectively abrogated SMAD4 binding, markedly reduced SMAD3 and 3+4 stimulation of the rFSHbeta gene promoter, and significantly decreased the synergistic enhancement of promoter activity by both activin A and GnRH, and SMAD3 and GnRH. |
| 375 | 15375186 | Blockade of the MAPK-signaling pathway did not significantly affect the response to combined stimulation with activin and GnRH. |
| 376 | 15375186 | In contrast, interference with SMAD3 signaling caused a significant reduction in activin and GnRH synergy. |
| 377 | 15375186 | The results indicate that SMAD3 plays an important role in the synergistic effects of activin and GnRH and demonstrate that this synergy is mediated by a palindromic cis-element located at -266/-259 of the rFSHbeta gene promoter. |
| 378 | 15512855 | Corticotrophin-releasing hormone (CRH) released during stress has been implicated in the disruption of the reproductive neuroendocrine axis, and 17beta-oestradiol (E2) has been shown to enhance stress-induced suppression of pulsatile gonadotrophin-releasing hormone (GnRH) and luteinising hormone (LH) release. |
| 379 | 15512855 | Suppression of LH pulses by insulin-induced hypoglycaemic (IIH) stress was completely prevented by intracerebroventricular (icv) administration of a CRH antagonist. |
| 380 | 15528398 | Hindbrain neurons producing neuropeptide Y (NPY) and catecholamines (CA) then project to the forebrain where they contact GnRH neurons both directly and also indirectly via corticotropin-releasing hormone (CRH) neurons to inhibit GnRH secretion. |
| 381 | 15528398 | In the case of estrous behavior, the best available evidence suggests that the inhibitory NPY/CA system acts primarily via CRH or urocortin projections to various forebrain loci that control sexual receptivity. |
| 382 | 15578334 | Recently however a second form of GnRH (GnRH-II) has been described in the human. |
| 383 | 15578334 | The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. |
| 384 | 15578334 | Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in normal B-LCLs. |
| 385 | 15578334 | GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. |
| 386 | 15578334 | Recently however a second form of GnRH (GnRH-II) has been described in the human. |
| 387 | 15578334 | The present study investigates GnRH-I and GnRH-II expression in human peripheral mononuclear blood cells (PMBCs) and B lymphoblastoid cells (B-LCLs), as well as their action in regulating B-LCL proliferation in the presence and absence of interleukin-2 (IL-2), both in GnRHR-I mutated lymphocytes and in a normal control. |
| 388 | 15578334 | Co-incubation of IL-2 and IL-2 + GnRH 10 (-5) M with a GnRH antagonist (Cetrorelix; 10 (-6) M) significantly attenuated the proliferation in normal B-LCLs. |
| 389 | 15578334 | GnRH-II did not affect proliferation of normal B-LCLs alone, and did not alter the proliferative response to IL-2. |
| 390 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 391 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 392 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 393 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 394 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 395 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 396 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 397 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 398 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 399 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 400 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 401 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 402 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 403 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 404 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 405 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 406 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 407 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 408 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 409 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 410 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 411 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 412 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 413 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 414 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 415 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 416 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 417 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 418 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 419 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 420 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 421 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 422 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 423 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 424 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 425 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 426 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 427 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 428 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 429 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 430 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 431 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 432 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 433 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 434 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 435 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 436 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 437 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 438 | 15662591 | Signal transduction mediating gene expression of SP1, LHbeta-subunit and GH in response to GnRH or GHRH in the postnatal and fetal porcine anterior pituitary in vitro. |
| 439 | 15662591 | To clarify signal transduction pathways mediating putative gene expression of transcription factor SP1 (selective promoter factor 1 or specificity protein 1) by GnRH or GHRH porcine anterior pituitary monolayer cultures were exposed for various time periods to GnRH, GHRH, activators of adenylate cyclase (AC) or proteinkinase C (PKC), and mRNA levels of SP1, LHbeta-subunit, and GH were determined by multiplex RT-PCR. |
| 440 | 15662591 | Postnatally (4 weeks) SP1 mRNA level was maximally increased by GnRH, GHRH and both by activation of AC or PKC after 2 h of exposure. |
| 441 | 15662591 | Two-hour stimulation of SP1 mRNA levels by dbcAMP was totally blocked by H89, while this inhibitor not clearly blocked GHRH stimulated SP1 mRNA levels. |
| 442 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 443 | 15662591 | Already at day 50 of fetal life (and likewise day 80) SP1 mRNA levels were stimulated by GHRH or activation of AC, but not by GnRH or activation of PKC. |
| 444 | 15662591 | The results are consistent with the notion that SP1 plays an important role 1) in conferring GnRH responsiveness to the LHbeta-subunit gene by mediating the actions of both AC and PKC and 2) in conferring GHRH responsiveness to the GH gene through activation of the AC probably PKA pathway. |
| 445 | 15662591 | Furthermore, the data are in line with the view that the GHRH/AC/SP1/GH pathway develops earlier during fetal life than the GnRH/PKC/SP1/LHbeta pathway. |
| 446 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 447 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 448 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 449 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 450 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 451 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 452 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 453 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 454 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 455 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 456 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 457 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 458 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 459 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 460 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 461 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 462 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 463 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 464 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 465 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 466 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 467 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 468 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 469 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 470 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 471 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 472 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 473 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 474 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 475 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 476 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 477 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 478 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 479 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 480 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 481 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 482 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 483 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 484 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 485 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 486 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 487 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 488 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 489 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 490 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 491 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 492 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 493 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 494 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 495 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 496 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 497 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 498 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 499 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 500 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 501 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 502 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 503 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 504 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 505 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 506 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 507 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 508 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 509 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 510 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 511 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 512 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 513 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 514 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 515 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 516 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 517 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 518 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 519 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 520 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 521 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 522 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 523 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 524 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 525 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 526 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 527 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 528 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 529 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 530 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 531 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 532 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 533 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 534 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 535 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 536 | 16141398 | Using a perifusion system, we previously reported that stimulation of the LbetaT2 cell line with varying GnRH pulse frequencies resulted in differential stimulation of LHbeta and FSHbeta gene transcription, analogous to previous observations in primary gonadotropes. |
| 537 | 16141398 | In the present study, we investigated the patterns of MAPK activation by GnRH and the role of MAPK in mediating the frequency-dependent effects. |
| 538 | 16141398 | In static culture, ERK activation in LbetaT2 cells stimulated with continuous GnRH (10 nM) was maximal by 10 min and persisted for up to 6 h, with a return to basal levels by 20 h. |
| 539 | 16141398 | In contrast, stimulation with continuous GnRH (10 nM) in perifused cells resulted in a more sustained activation of ERK. |
| 540 | 16141398 | To investigate the effects of GnRH pulse frequency on ERK activation, perifused LbetaT2 cells were stimulated with pulsatile GnRH at a frequency of one pulse every 30 min or one pulse every 2 h for 20 h (10 nM, 5 min/pulse). |
| 541 | 16141398 | After the final GnRH pulse, cells were lysed at frequent intervals and levels of ERK phosphorylation were measured. |
| 542 | 16141398 | Under high-frequency conditions, ERK activation was maximal 10 min after the GnRH pulse and returned to baseline levels by 20 min. |
| 543 | 16141398 | In contrast, under lower GnRH pulse frequency conditions, ERK activation occurred more rapidly and activation was more sustained, with a slower rate of ERK dephosphorylation. |
| 544 | 16141398 | Blockade of ERK activation abolished GnRH-dependent activation of LHbeta and FSHbeta transcription at both high and low pulse frequencies. |
| 545 | 16141398 | These results demonstrate that in perifused LbetaT2 cells, distinct patterns of ERK activation/inactivation are regulated by GnRH pulse frequency, and the difference in ERK activation may be important for GnRH pulse frequency-dependent differential stimulation of LHbeta and FSHbeta gene expression. |
| 546 | 16926523 | Basal plasma levels of GH and insulin-like growth factor-I under fasting hyperglycemia (202 mg/dl) were markedly elevated. |
| 547 | 16926523 | Plasma GH levels paradoxically increased after stimulation with TRH and LH-RH, and decreased after bromocriptine and octreotide administration. |
| 548 | 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. |
| 549 | 17003237 | Calcium receptor stimulates chemotaxis and secretion of MCP-1 in GnRH neurons in vitro: potential impact on reduced GnRH neuron population in CaR-null mice. |
| 550 | 17003237 | We studied whether the extracellular calcium-sensing receptor (CaR) promotes migration/chemotaxis of GnRH neurons. |
| 551 | 17003237 | We also demonstrated expression of a beta-chemokine, monocyte chemoattractant protein-1 (MCP-1), and its receptor, CC motif receptor-2 (CCR2), in the hypothalamic GnRH neurons as well as in GT1-7 and GN11 cells. |
| 552 | 17003237 | Exogenous MCP-1 stimulated chemotaxis of both cell lines in a dose-dependent fashion; the effect was greater in GN11 than in GT1-7 cells, consistent with the higher CCR2 mRNA levels in GN11 cells. |
| 553 | 17003237 | We conclude that the CaR may be a novel regulator of GnRH neuronal migration likely involving, in part, MCP-1. |
| 554 | 17003237 | Calcium receptor stimulates chemotaxis and secretion of MCP-1 in GnRH neurons in vitro: potential impact on reduced GnRH neuron population in CaR-null mice. |
| 555 | 17003237 | We studied whether the extracellular calcium-sensing receptor (CaR) promotes migration/chemotaxis of GnRH neurons. |
| 556 | 17003237 | We also demonstrated expression of a beta-chemokine, monocyte chemoattractant protein-1 (MCP-1), and its receptor, CC motif receptor-2 (CCR2), in the hypothalamic GnRH neurons as well as in GT1-7 and GN11 cells. |
| 557 | 17003237 | Exogenous MCP-1 stimulated chemotaxis of both cell lines in a dose-dependent fashion; the effect was greater in GN11 than in GT1-7 cells, consistent with the higher CCR2 mRNA levels in GN11 cells. |
| 558 | 17003237 | We conclude that the CaR may be a novel regulator of GnRH neuronal migration likely involving, in part, MCP-1. |
| 559 | 17003237 | Calcium receptor stimulates chemotaxis and secretion of MCP-1 in GnRH neurons in vitro: potential impact on reduced GnRH neuron population in CaR-null mice. |
| 560 | 17003237 | We studied whether the extracellular calcium-sensing receptor (CaR) promotes migration/chemotaxis of GnRH neurons. |
| 561 | 17003237 | We also demonstrated expression of a beta-chemokine, monocyte chemoattractant protein-1 (MCP-1), and its receptor, CC motif receptor-2 (CCR2), in the hypothalamic GnRH neurons as well as in GT1-7 and GN11 cells. |
| 562 | 17003237 | Exogenous MCP-1 stimulated chemotaxis of both cell lines in a dose-dependent fashion; the effect was greater in GN11 than in GT1-7 cells, consistent with the higher CCR2 mRNA levels in GN11 cells. |
| 563 | 17003237 | We conclude that the CaR may be a novel regulator of GnRH neuronal migration likely involving, in part, MCP-1. |
| 564 | 17003237 | Calcium receptor stimulates chemotaxis and secretion of MCP-1 in GnRH neurons in vitro: potential impact on reduced GnRH neuron population in CaR-null mice. |
| 565 | 17003237 | We studied whether the extracellular calcium-sensing receptor (CaR) promotes migration/chemotaxis of GnRH neurons. |
| 566 | 17003237 | We also demonstrated expression of a beta-chemokine, monocyte chemoattractant protein-1 (MCP-1), and its receptor, CC motif receptor-2 (CCR2), in the hypothalamic GnRH neurons as well as in GT1-7 and GN11 cells. |
| 567 | 17003237 | Exogenous MCP-1 stimulated chemotaxis of both cell lines in a dose-dependent fashion; the effect was greater in GN11 than in GT1-7 cells, consistent with the higher CCR2 mRNA levels in GN11 cells. |
| 568 | 17003237 | We conclude that the CaR may be a novel regulator of GnRH neuronal migration likely involving, in part, MCP-1. |
| 569 | 17018449 | Recent data suggest that in addition to leptin's role in conveying signals of the amount of energy stores to the central nervous system, this adipocyte secreted hormone interacts with the endocrine system to provide critical information about the size of fat stores, acting as a permissive factor that allows the triggering of energy demanding situations as the onset of puberty and reproduction. |
| 570 | 17018449 | The hypothalamus is an important site of leptin's action where a complex network of neuropeptides is involved in leptin's effect on GnRH. |
| 571 | 17213356 | The ovarian-type stroma had a spindle cell component that was positive for progesterone receptors and had the hitherto unreported presence of abundant foci of luteinised stromal cells with characteristic immunohistochemical positivity to alpha-inhibin, calretinin, aromatase and gonadotropin-releasing hormone (GnRH) receptors. |
| 572 | 17476303 | Administration of kisspeptin-10 resulted in an increase in plasma luteinizing hormone levels, further supporting appropriate regulation of the introduced GnRH transgene. |
| 573 | 17710734 | Folliculostellate cells are targets of cytokines, peptides, and steroid hormones, and produce growth factors and cytokines, including follistatin, the dynamic regulator of follicle-stimulating hormone (FSH) production that binds activin, and limits activin signaling. |
| 574 | 17710734 | Pituitary adenylate cyclase-activating peptide (PACAP) and its receptor are found in folliculostellate cells in which they stimulate transcription of the follistatin gene through cyclic adenosine monophosphate/protein kinase A (PKA) signaling. |
| 575 | 17710734 | When PACAP increases, follistatin levels increase, and FSH-beta mRNA is reduced. |
| 576 | 17710734 | PACAP also activates gonadotrophs to stimulate transcription of the gonadotropin alpha-subunit gene and lengthen the LH-beta mRNA, presumably to prolong it half-life, and increases responsiveness to GnRH. |
| 577 | 17985235 | Interactions between TNF and GnRH. |
| 578 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 579 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 580 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 581 | 17985235 | Interactions between TNF and GnRH. |
| 582 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 583 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 584 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 585 | 17985235 | Interactions between TNF and GnRH. |
| 586 | 17985235 | Tumour necrosis factor (TNF) ligand members and their associated TNF receptor (TNFR) superfamilies have many diverse physiological roles. |
| 587 | 17985235 | The cellular signalling machinery used by TNFRs to achieve their many cellular responses are discussed, as is the gonadotrophin-releasing hormone (GnRH) receptor signalling mechanisms. |
| 588 | 17985235 | These interactions between TNF, GnRH and gonadotrophs are discussed. |
| 589 | 18463157 | Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH). |
| 590 | 18463157 | Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS. |
| 591 | 18463157 | Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions. |
| 592 | 18463157 | Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS. |
| 593 | 18463157 | Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH). |
| 594 | 18463157 | Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS. |
| 595 | 18463157 | Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions. |
| 596 | 18463157 | Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS. |
| 597 | 18463157 | Idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann syndrome (KS) are clinically and genetically heterogeneous disorders caused by a deficiency of gonadotrophin-releasing hormone (GnRH). |
| 598 | 18463157 | Mutations in three genes--KAL1, GNRHR and FGFR1--account for 15-20% of all causes of IHH/KS. |
| 599 | 18463157 | Fifty-four IHH/KS patients were studied for KAL1 deletions and 100 were studied for an autosomal panel of FGFR1, GNRH1, GNRHR, GPR54 and NELF gene deletions. |
| 600 | 18463157 | Our results indicate approximately 12% of KS males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in IHH/KS. |
| 601 | 18499748 | The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice. |
| 602 | 18499748 | In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron. |
| 603 | 18499748 | Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons. |
| 604 | 18499748 | Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts. |
| 605 | 18499748 | The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice. |
| 606 | 18499748 | In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron. |
| 607 | 18499748 | Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons. |
| 608 | 18499748 | Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts. |
| 609 | 18499748 | The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice. |
| 610 | 18499748 | In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron. |
| 611 | 18499748 | Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons. |
| 612 | 18499748 | Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts. |
| 613 | 18499748 | The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice. |
| 614 | 18499748 | In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron. |
| 615 | 18499748 | Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons. |
| 616 | 18499748 | Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts. |
| 617 | 18550775 | Although FSH plays an essential role in controlling gametogenesis, the biology of FSHbeta transcription remains poorly understood, but is known to involve the complex interplay of multiple endocrine factors including GnRH. |
| 618 | 18550775 | We have identified a GnRH-responsive element within the rat FSHbeta promoter containing an E-box and partial cAMP response element site that are bound by the basic helix loop helix transcription factor family members, upstream stimulating factor (USF)-1/USF-2, and the basic leucine zipper member, cAMP response element-binding protein (CREB), respectively. |
| 619 | 18550775 | Expression studies with CREB, USF-1/USF-2, and activating protein-1 demonstrated that the USF transcription factors increased basal transcription, an effect not observed if the cognate binding site was mutated. |
| 620 | 18550775 | Conversely, expression of a dominant negative CREB mutant or CREB knockdown attenuated induction by GnRH, whereas dominant negative Fos or USF had no effect on the GnRH response. |
| 621 | 18550775 | GnRH stimulation specifically induced an increase in phosphorylated CREB occupation of the FSHbeta promoter, leading to the recruitment of CREB-binding protein to enhance gene transcription. |
| 622 | 18550775 | In conclusion, a composite element bound by both USF and CREB serves to integrate signals for basal and GnRH-stimulated transcription of the rat FSHbeta gene. |
| 623 | 18550775 | Although FSH plays an essential role in controlling gametogenesis, the biology of FSHbeta transcription remains poorly understood, but is known to involve the complex interplay of multiple endocrine factors including GnRH. |
| 624 | 18550775 | We have identified a GnRH-responsive element within the rat FSHbeta promoter containing an E-box and partial cAMP response element site that are bound by the basic helix loop helix transcription factor family members, upstream stimulating factor (USF)-1/USF-2, and the basic leucine zipper member, cAMP response element-binding protein (CREB), respectively. |
| 625 | 18550775 | Expression studies with CREB, USF-1/USF-2, and activating protein-1 demonstrated that the USF transcription factors increased basal transcription, an effect not observed if the cognate binding site was mutated. |
| 626 | 18550775 | Conversely, expression of a dominant negative CREB mutant or CREB knockdown attenuated induction by GnRH, whereas dominant negative Fos or USF had no effect on the GnRH response. |
| 627 | 18550775 | GnRH stimulation specifically induced an increase in phosphorylated CREB occupation of the FSHbeta promoter, leading to the recruitment of CREB-binding protein to enhance gene transcription. |
| 628 | 18550775 | In conclusion, a composite element bound by both USF and CREB serves to integrate signals for basal and GnRH-stimulated transcription of the rat FSHbeta gene. |
| 629 | 18550775 | Although FSH plays an essential role in controlling gametogenesis, the biology of FSHbeta transcription remains poorly understood, but is known to involve the complex interplay of multiple endocrine factors including GnRH. |
| 630 | 18550775 | We have identified a GnRH-responsive element within the rat FSHbeta promoter containing an E-box and partial cAMP response element site that are bound by the basic helix loop helix transcription factor family members, upstream stimulating factor (USF)-1/USF-2, and the basic leucine zipper member, cAMP response element-binding protein (CREB), respectively. |
| 631 | 18550775 | Expression studies with CREB, USF-1/USF-2, and activating protein-1 demonstrated that the USF transcription factors increased basal transcription, an effect not observed if the cognate binding site was mutated. |
| 632 | 18550775 | Conversely, expression of a dominant negative CREB mutant or CREB knockdown attenuated induction by GnRH, whereas dominant negative Fos or USF had no effect on the GnRH response. |
| 633 | 18550775 | GnRH stimulation specifically induced an increase in phosphorylated CREB occupation of the FSHbeta promoter, leading to the recruitment of CREB-binding protein to enhance gene transcription. |
| 634 | 18550775 | In conclusion, a composite element bound by both USF and CREB serves to integrate signals for basal and GnRH-stimulated transcription of the rat FSHbeta gene. |
| 635 | 18550775 | Although FSH plays an essential role in controlling gametogenesis, the biology of FSHbeta transcription remains poorly understood, but is known to involve the complex interplay of multiple endocrine factors including GnRH. |
| 636 | 18550775 | We have identified a GnRH-responsive element within the rat FSHbeta promoter containing an E-box and partial cAMP response element site that are bound by the basic helix loop helix transcription factor family members, upstream stimulating factor (USF)-1/USF-2, and the basic leucine zipper member, cAMP response element-binding protein (CREB), respectively. |
| 637 | 18550775 | Expression studies with CREB, USF-1/USF-2, and activating protein-1 demonstrated that the USF transcription factors increased basal transcription, an effect not observed if the cognate binding site was mutated. |
| 638 | 18550775 | Conversely, expression of a dominant negative CREB mutant or CREB knockdown attenuated induction by GnRH, whereas dominant negative Fos or USF had no effect on the GnRH response. |
| 639 | 18550775 | GnRH stimulation specifically induced an increase in phosphorylated CREB occupation of the FSHbeta promoter, leading to the recruitment of CREB-binding protein to enhance gene transcription. |
| 640 | 18550775 | In conclusion, a composite element bound by both USF and CREB serves to integrate signals for basal and GnRH-stimulated transcription of the rat FSHbeta gene. |
| 641 | 18550775 | Although FSH plays an essential role in controlling gametogenesis, the biology of FSHbeta transcription remains poorly understood, but is known to involve the complex interplay of multiple endocrine factors including GnRH. |
| 642 | 18550775 | We have identified a GnRH-responsive element within the rat FSHbeta promoter containing an E-box and partial cAMP response element site that are bound by the basic helix loop helix transcription factor family members, upstream stimulating factor (USF)-1/USF-2, and the basic leucine zipper member, cAMP response element-binding protein (CREB), respectively. |
| 643 | 18550775 | Expression studies with CREB, USF-1/USF-2, and activating protein-1 demonstrated that the USF transcription factors increased basal transcription, an effect not observed if the cognate binding site was mutated. |
| 644 | 18550775 | Conversely, expression of a dominant negative CREB mutant or CREB knockdown attenuated induction by GnRH, whereas dominant negative Fos or USF had no effect on the GnRH response. |
| 645 | 18550775 | GnRH stimulation specifically induced an increase in phosphorylated CREB occupation of the FSHbeta promoter, leading to the recruitment of CREB-binding protein to enhance gene transcription. |
| 646 | 18550775 | In conclusion, a composite element bound by both USF and CREB serves to integrate signals for basal and GnRH-stimulated transcription of the rat FSHbeta gene. |
| 647 | 19075678 | It has also been shown that insulin facilitates the secretion of gonadotrophin releasing hormone (GnRH) from neuronal cell cultures. |
| 648 | 19075678 | Thus, HH may be the result of insulin resistance at the level of the GnRH secreting neuron. |
| 649 | 19075678 | It has also been shown that insulin facilitates the secretion of gonadotrophin releasing hormone (GnRH) from neuronal cell cultures. |
| 650 | 19075678 | Thus, HH may be the result of insulin resistance at the level of the GnRH secreting neuron. |
| 651 | 19282386 | The GnRH receptor (GnRHR) responds to pulsatile GnRH signals to coordinate pituitary gonadotropin synthesis and secretion. |
| 652 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 653 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 654 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 655 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 656 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 657 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 658 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 659 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 660 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 661 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 662 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 663 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 664 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 665 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 666 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 667 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 668 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 669 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 670 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 671 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 672 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 673 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 674 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 675 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 676 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 677 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 678 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 679 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 680 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 681 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 682 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 683 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 684 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 685 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 686 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 687 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 688 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 689 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 690 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 691 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 692 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 693 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 694 | 19669946 | Our experiment investigated the mRNA expression of intestinal gonadotropin-releasing hormone (GnRH), proglucagon (PG), and glucagon-like peptide 1 receptor (GLP-1R) in the jejunum, ileum, and colon of rats fed with high-fat diet and Goto-Kakizaki (GK) rats and revealed the physiological role of intestinal GnRH. |
| 695 | 19669946 | However, the GnRH receptor (GnRHR) and GLP-1R mRNA levels did not differ significantly between HCh and control. |
| 696 | 19669946 | The GnRH, PG, and GLP-1R mRNA levels in GK rats were lower, respectively, than those in control rats, while the GnRHR levels did not differ significantly between GK rats and control rats. |
| 697 | 19669946 | There were no difference in GnRH, PG, GnRHR, and GLP-1R mRNA levels in the ileum and colon tissue between HCh and control rats. |
| 698 | 19669946 | The GnRH mRNA levels of GK rats were lower than those in control rats; however, the PG, GLP-1R, and GnRHR levels did not differ significantly between GK and control rats. |
| 699 | 19669946 | The GnRH level in the jejunum showed a significant effect on blood glucose level, while the PG level in the jejunum showed a significant effect on insulin level. |
| 700 | 19669946 | This may imply that, compared with the ileum and colon, the jejunum had greater impact on glucose metabolism; furthermore, GnRH might interact with intestinal GLP-1 and GLP-2 through the paracrine and autocrine ways and then regulate glucose metabolism and insulin secretion. |
| 701 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 702 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 703 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 704 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 705 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 706 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 707 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 708 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 709 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 710 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 711 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 712 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 713 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 714 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 715 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 716 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 717 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 718 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 719 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 720 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 721 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 722 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 723 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 724 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 725 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 726 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 727 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 728 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 729 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 730 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 731 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 732 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 733 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 734 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 735 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 736 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 737 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 738 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 739 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 740 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 741 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 742 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 743 | 20008557 | Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility. |
| 744 | 20008557 | In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH. |
| 745 | 20008557 | In this study, mutation of a cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential GnRH stimulation at low pulse frequencies. |
| 746 | 20008557 | We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role. |
| 747 | 20008557 | ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies. |
| 748 | 20008557 | ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription. |
| 749 | 20008557 | These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function. |
| 750 | 20689830 | Reproductive hormone-dependent and -independent contributions to developmental changes in kisspeptin in GnRH-deficient hypogonadal mice. |
| 751 | 20689830 | Kisspeptin is a potent activator of GnRH-induced gonadotropin secretion and is a proposed central regulator of pubertal onset. |
| 752 | 20689830 | In order to better understand sex steroid hormone-dependent and -independent effects on the maturation of kisspeptin neurons, hypogonadal (hpg) mice deficient in GnRH and its downstream effectors were used to determine changes in the developmental kisspeptin expression. |
| 753 | 20689830 | Reproductive hormone-dependent and -independent contributions to developmental changes in kisspeptin in GnRH-deficient hypogonadal mice. |
| 754 | 20689830 | Kisspeptin is a potent activator of GnRH-induced gonadotropin secretion and is a proposed central regulator of pubertal onset. |
| 755 | 20689830 | In order to better understand sex steroid hormone-dependent and -independent effects on the maturation of kisspeptin neurons, hypogonadal (hpg) mice deficient in GnRH and its downstream effectors were used to determine changes in the developmental kisspeptin expression. |
| 756 | 20689830 | Reproductive hormone-dependent and -independent contributions to developmental changes in kisspeptin in GnRH-deficient hypogonadal mice. |
| 757 | 20689830 | Kisspeptin is a potent activator of GnRH-induced gonadotropin secretion and is a proposed central regulator of pubertal onset. |
| 758 | 20689830 | In order to better understand sex steroid hormone-dependent and -independent effects on the maturation of kisspeptin neurons, hypogonadal (hpg) mice deficient in GnRH and its downstream effectors were used to determine changes in the developmental kisspeptin expression. |
| 759 | 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. |
| 760 | 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. |
| 761 | 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. |
| 762 | 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. |
| 763 | 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. |
| 764 | 21076077 | Peroxisome proliferators-activated receptor gamma (PPARG) ligands improve insulin sensitivity in type 2 diabetes and polycystic ovarian syndrome (PCOS). |
| 765 | 21076077 | Despite clinical studies showing normalization of pituitary responsiveness to gonadotropin-releasing hormone (GnRH) in patients with PCOS, the precise role of PPARG in regulating the hypothalamic-pituitary-gonadal axis remains unclear. |
| 766 | 21076077 | In mouse LbetaT2 immortalized gonadotrophs, rosiglitazone treatment inhibited GnRH stimulation of the stress kinases p38MAPK and MAPKs/JNKs, but did not alter activation of ERKs, both in the presence and absence of activin. |
| 767 | 21076077 | Furthermore, p38MAPK signaling was critical for both Lhb and Fshb promoter activity, and rosiglitazone suppressed the GnRH-mediated induction of Lhb and Fshb mRNA. |
| 768 | 21076077 | Depletion of PPARG using a lentivirally encoded short hairpin RNA abolishes the effect of rosiglitazone to suppress activation of JNKs and induction of the transcription factors EGR1 and FOS as well as the gonadotropin genes Lhb and Fshb. |
| 769 | 21076077 | Lastly, we show conditional knockout of Pparg in pituitary gonadotrophs caused an increase in luteinizing hormone levels in female mice, a decrease in follicle-stimulating hormone in male mice, and a fertility defect characterized by reduced litter size. |
| 770 | 21076077 | Peroxisome proliferators-activated receptor gamma (PPARG) ligands improve insulin sensitivity in type 2 diabetes and polycystic ovarian syndrome (PCOS). |
| 771 | 21076077 | Despite clinical studies showing normalization of pituitary responsiveness to gonadotropin-releasing hormone (GnRH) in patients with PCOS, the precise role of PPARG in regulating the hypothalamic-pituitary-gonadal axis remains unclear. |
| 772 | 21076077 | In mouse LbetaT2 immortalized gonadotrophs, rosiglitazone treatment inhibited GnRH stimulation of the stress kinases p38MAPK and MAPKs/JNKs, but did not alter activation of ERKs, both in the presence and absence of activin. |
| 773 | 21076077 | Furthermore, p38MAPK signaling was critical for both Lhb and Fshb promoter activity, and rosiglitazone suppressed the GnRH-mediated induction of Lhb and Fshb mRNA. |
| 774 | 21076077 | Depletion of PPARG using a lentivirally encoded short hairpin RNA abolishes the effect of rosiglitazone to suppress activation of JNKs and induction of the transcription factors EGR1 and FOS as well as the gonadotropin genes Lhb and Fshb. |
| 775 | 21076077 | Lastly, we show conditional knockout of Pparg in pituitary gonadotrophs caused an increase in luteinizing hormone levels in female mice, a decrease in follicle-stimulating hormone in male mice, and a fertility defect characterized by reduced litter size. |
| 776 | 21076077 | Peroxisome proliferators-activated receptor gamma (PPARG) ligands improve insulin sensitivity in type 2 diabetes and polycystic ovarian syndrome (PCOS). |
| 777 | 21076077 | Despite clinical studies showing normalization of pituitary responsiveness to gonadotropin-releasing hormone (GnRH) in patients with PCOS, the precise role of PPARG in regulating the hypothalamic-pituitary-gonadal axis remains unclear. |
| 778 | 21076077 | In mouse LbetaT2 immortalized gonadotrophs, rosiglitazone treatment inhibited GnRH stimulation of the stress kinases p38MAPK and MAPKs/JNKs, but did not alter activation of ERKs, both in the presence and absence of activin. |
| 779 | 21076077 | Furthermore, p38MAPK signaling was critical for both Lhb and Fshb promoter activity, and rosiglitazone suppressed the GnRH-mediated induction of Lhb and Fshb mRNA. |
| 780 | 21076077 | Depletion of PPARG using a lentivirally encoded short hairpin RNA abolishes the effect of rosiglitazone to suppress activation of JNKs and induction of the transcription factors EGR1 and FOS as well as the gonadotropin genes Lhb and Fshb. |
| 781 | 21076077 | Lastly, we show conditional knockout of Pparg in pituitary gonadotrophs caused an increase in luteinizing hormone levels in female mice, a decrease in follicle-stimulating hormone in male mice, and a fertility defect characterized by reduced litter size. |
| 782 | 21664428 | In 2003, Fibroblast growth factor receptor 1 (FGFR1) was discovered as a novel locus causing both forms of isolate GnRH Deficiency, Kallmann syndrome [KS with anosmia] and normosmic idiopathic hypogonadotropic hypogonadism [nIHH] eventually accounting for approximately 10% of gonadotropin-releasing hormone (GnRH) deficiency cases. |
| 783 | 21664428 | Additionally, the variable expressivity of both reproductive and non-reproductive phenotypes among patients and family members harboring the identical FGFR1 mutations has pointed to a more complex, oligogenic model for GnRH deficiency. |
| 784 | 21664428 | Further, reversal of HH in patients carrying FGFR1 mutations suggests potential gene-environment interactions in human GnRH deficiency disorders. |
| 785 | 21664428 | In 2003, Fibroblast growth factor receptor 1 (FGFR1) was discovered as a novel locus causing both forms of isolate GnRH Deficiency, Kallmann syndrome [KS with anosmia] and normosmic idiopathic hypogonadotropic hypogonadism [nIHH] eventually accounting for approximately 10% of gonadotropin-releasing hormone (GnRH) deficiency cases. |
| 786 | 21664428 | Additionally, the variable expressivity of both reproductive and non-reproductive phenotypes among patients and family members harboring the identical FGFR1 mutations has pointed to a more complex, oligogenic model for GnRH deficiency. |
| 787 | 21664428 | Further, reversal of HH in patients carrying FGFR1 mutations suggests potential gene-environment interactions in human GnRH deficiency disorders. |
| 788 | 21664428 | In 2003, Fibroblast growth factor receptor 1 (FGFR1) was discovered as a novel locus causing both forms of isolate GnRH Deficiency, Kallmann syndrome [KS with anosmia] and normosmic idiopathic hypogonadotropic hypogonadism [nIHH] eventually accounting for approximately 10% of gonadotropin-releasing hormone (GnRH) deficiency cases. |
| 789 | 21664428 | Additionally, the variable expressivity of both reproductive and non-reproductive phenotypes among patients and family members harboring the identical FGFR1 mutations has pointed to a more complex, oligogenic model for GnRH deficiency. |
| 790 | 21664428 | Further, reversal of HH in patients carrying FGFR1 mutations suggests potential gene-environment interactions in human GnRH deficiency disorders. |
| 791 | 22229029 | Developmental defects of GnRH neurons and the olfactory bulb are associated with hyposmia, rarely associated with the clinical phenotypes of synkinesia, cleft palate, ear anomalies, or choanal atresia, and may be due to mutations of KAL1, FGFR1/FGF8, PROKR2/PROK2, or CHD7. |
| 792 | 22229029 | Impaired GnRH secretion in normosmic patients with IHH may be caused by deficient hypothalamic GPR54/KISS1, TACR3/TAC3, and leptinR/leptin signalling or mutations within the GNRH1 gene itself. |
| 793 | 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). |
| 794 | 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. |
| 795 | 23392256 | Delayed puberty but normal fertility in mice with selective deletion of insulin receptors from Kiss1 cells. |
| 796 | 23392256 | The neuropeptide kisspeptin, encoded by the Kiss1 gene, modifies GnRH neuronal activity to initiate puberty and maintain fertility, but the factors that regulate Kiss1 neurons and permit pubertal maturation remain to be clarified. |
| 797 | 23392256 | To determine whether insulin sensing plays an important role in Kiss1 neuron function, we generated mice lacking insulin receptors in Kiss1 neurons (IR(ΔKiss) mice). |
| 798 | 23392256 | These data suggest that impaired insulin sensing by Kiss1 neurons delays the initiation of puberty but does not affect adult fertility. |
| 799 | 23393127 | Expression of pituitary FSH and LH, under the control of pulsatile GnRH, is essential for fertility. cAMP response element-binding protein (CREB) has been implicated in the regulation of FSHβ gene expression, but the molecular mechanisms by which pulsatile GnRH regulates CREB activation remain poorly understood. |
| 800 | 23393127 | GnRH stimulation of CREB phosphorylation (pCREB) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (PKA) inhibitor, H89. |