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Gene Information
Gene symbol: GHRH
Gene name: growth hormone releasing hormone
HGNC ID: 4265
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1306783 | [Blunted growth hormone response to hGRF 1-29 NH2 in patients with non-insulin-dependent diabetes mellitus]. |
| 2 | 1306783 | There exists some defect in central GH control in diabetics with enhanced somatostatin secretion and abnormal sensitivity of the GH secretion cells to a variety of regulatory factors including GRF, glucose, amino-acids, free fat acid. |
| 3 | 1306783 | [Blunted growth hormone response to hGRF 1-29 NH2 in patients with non-insulin-dependent diabetes mellitus]. |
| 4 | 1306783 | There exists some defect in central GH control in diabetics with enhanced somatostatin secretion and abnormal sensitivity of the GH secretion cells to a variety of regulatory factors including GRF, glucose, amino-acids, free fat acid. |
| 5 | 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. |
| 6 | 1350066 | In an attempt to determine if increased somatostatin (SRIF) secretion is responsible for the decreased GH secretion, we studied the effect of modulating SRIF tone on the GH response to GHRH in normal and streptozotocin-induced diabetic rats. |
| 7 | 1350066 | Rats were pretreated with either normal sheep serum and saline (NSS+SAL), somatostatin antibodies (SRIF-Ab), or pyridostigmine (PD), an acetylcholinesterase inhibitor hypothesized to reduce hypothalamic SRIF secretion. |
| 8 | 1350067 | In the present study we investigated the effects of modulating endogenous somatostatin (SRIF) on the GH response to growth hormone-releasing hormone (GHRH) in spontaneously diabetic BB/Wor rats and nondiabetic littermates. |
| 9 | 1350067 | Plasma growth hormone (GH) concentrations following injection of GHRH (500 ng/kg, i.v.) were measured in the rats after pretreatment with either normal sheep serum+saline (NSS+SAL), somatostatin antibody (SRIF-Ab), or pyridostigmine bromide (PD), an acetylcholine esterase inhibitor hypothesized to decrease hypothalamic SRIF tone. |
| 10 | 1350067 | In the present study we investigated the effects of modulating endogenous somatostatin (SRIF) on the GH response to growth hormone-releasing hormone (GHRH) in spontaneously diabetic BB/Wor rats and nondiabetic littermates. |
| 11 | 1350067 | Plasma growth hormone (GH) concentrations following injection of GHRH (500 ng/kg, i.v.) were measured in the rats after pretreatment with either normal sheep serum+saline (NSS+SAL), somatostatin antibody (SRIF-Ab), or pyridostigmine bromide (PD), an acetylcholine esterase inhibitor hypothesized to decrease hypothalamic SRIF tone. |
| 12 | 1355581 | Corticotropin-releasing hormone inhibition of paradoxical growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics. |
| 13 | 1355581 | A paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) has been observed in type 1 diabetic patients and was hypothetically attributed to a reduced hypothalamic somatostatin tone. |
| 14 | 1355581 | We have previously reported that corticotropin-releasing hormone (CRH) inhibits GH response to growth hormone-releasing hormone (GHRH) in normal subjects, possibly by an increased release of somatostatin. |
| 15 | 1355581 | To study the effect of CRH on anomalous GH response to TRH, we tested with TRH (200 micrograms intravenously [IV]) and CRH (100 micrograms IV) + TRH (200 micrograms IV) 13 patients (six males and seven women) affected by insulin-dependent diabetes mellitus. |
| 16 | 1355581 | In these subjects, the simultaneous administration of CRH and TRH significantly reduced the GH response to TRH, as assessed by both the maximal GH mean peak +/- SE (2.18 +/- 0.67 v 9.2 +/- 1.26 micrograms/L, P less than 0.005) and the area under the curve (AUC) +/- SE (187 +/- 32 v 567 +/- 35 micrograms.min/L, P less than .001). |
| 17 | 1355581 | CRH had no effect on TRH-induced thyroid-stimulating hormone (TSH) release. |
| 18 | 1355581 | Our data demonstrate that the paradoxical GH response to TRH in patients with type 1 diabetes mellitus is blocked by CRH administration. |
| 19 | 1355581 | This CRH action may be due to an enhanced somatostatin release. |
| 20 | 1355581 | Our data also show that exogenous CRH has no effect on TSH response to TRH, thus suggesting the existence of separate pathways in the neuroregulation of GH and TSH secretion. |
| 21 | 1518441 | Particularly in the ectopic growth hormone-releasing hormone (GHRH) syndrome, Sandostatin is unequivocally effective and, in the ectopic corticotropin syndrome selected cases can be treated successfully with Sandostatin, leading to marked clinical improvement. |
| 22 | 1519429 | Effects of growth hormone releasing hormone on insulin action and insulin secretion in a hypopituitary patient evaluated by the clamp technique. |
| 23 | 1519429 | The effect of growth hormone releasing hormone (GHRH-44) therapy on insulin action and secretion was evaluated in a hypopituitary patient after one month and one year of treatment. |
| 24 | 1519429 | Effects of growth hormone releasing hormone on insulin action and insulin secretion in a hypopituitary patient evaluated by the clamp technique. |
| 25 | 1519429 | The effect of growth hormone releasing hormone (GHRH-44) therapy on insulin action and secretion was evaluated in a hypopituitary patient after one month and one year of treatment. |
| 26 | 1591027 | We reported a 16-year-old boy suffering from dwarfism, diabetes insipidus and progressive cerebellar ataxia. |
| 27 | 1591027 | Pituitary hormones (GH and ACTH) sufficiently responded to the loading of hypothalamic hormones such as growth hormone releasing factor and corticotropin releasing factor, in spite of poor responses of GH under the insulin stimulation or sleep. |
| 28 | 1600349 | Fourteen patients, including 3 with deletions of the mitochondrial DNA, had various and often multiple endocrine abnormalities: 6 patients were of short stature, 3 had irregular menstrual cycles, 3 had undersized testicles, 5 showed an insufficient rise of growth hormone following the administration of growth-hormone-releasing hormone, 4 showed an insufficient rise in FSH after administration of gonadotropin-releasing hormone, 5 had manifest diabetes mellitus, 3 showed an impaired glucose tolerance, and 2 patients had subnormal serum levels of parathormone in combination with hypocalcaemia. |
| 29 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 30 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 31 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 32 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 33 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 34 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 35 | 1678493 | Hypothalamic secretion of somatostatin and growth hormone-releasing factor into the hypophysial-portal circulation is reduced in streptozotocin diabetic male rats. |
| 36 | 1678493 | Alterations in hypothalamic growth hormone-releasing factor (GRF) or hypothalamic somatostatin (SRIF) secretion, increased systemic SRIF secretion, and changes in somatotroph sensitivity to these hypothalamic factors have been advanced as potential underlying mechanisms for the observed attenuation of GH secretion after STZ treatment. |
| 37 | 1678493 | Hypothalamic secretion of somatostatin and growth hormone-releasing factor into the hypophysial-portal circulation is reduced in streptozotocin diabetic male rats. |
| 38 | 1678493 | Alterations in hypothalamic growth hormone-releasing factor (GRF) or hypothalamic somatostatin (SRIF) secretion, increased systemic SRIF secretion, and changes in somatotroph sensitivity to these hypothalamic factors have been advanced as potential underlying mechanisms for the observed attenuation of GH secretion after STZ treatment. |
| 39 | 1682193 | The effect of continuous infusions of somatostatin (SRIF) on growth hormone (GH) secretion induced by GH-releasing hormone (GHRH) bolus was compared in a dose-response manner between diabetic subjects in poor glycemic control and nondiabetic subjects to address the hypothesis that altered pituitary responsiveness to SRIF contributes to the hypersecretion of GH in diabetes mellitus in humans. |
| 40 | 1682193 | In diabetic subjects after 2 wk of intensive insulin management, the change in the dose-response curve persisted despite significant decrements in glycosylated hemoglobin and increments in plasma insulinlike growth factor I. |
| 41 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 42 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 43 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 44 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 45 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 46 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 47 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 48 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 49 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 50 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 51 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 52 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 53 | 1686555 | Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. |
| 54 | 1686555 | The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. |
| 55 | 1686555 | There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. |
| 56 | 1686555 | This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. |
| 57 | 1715850 | Transferrin- and albumin-directed expression of growth-related peptides in transgenic sheep. |
| 58 | 1715850 | Chimeric genes containing either the mouse transferrin (Trf) enhancer/promoter fused to the structural sequences encoding bovine growth hormone (GH) or the mouse albumin (Alb) enhancer/promoter fused to the gene for human growth hormone-releasing factor (GRF) were microinjected into sheep zygotes. |
| 59 | 1715850 | In addition, elevated levels of circulating insulin-like growth factor-I were observed in the bovine GH-expressing Trf transgenic sheep. |
| 60 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 61 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 62 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 63 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 64 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 65 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 66 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 67 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 68 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 69 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 70 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 71 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 72 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 73 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 74 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 75 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 76 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 77 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 78 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 79 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 80 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 81 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 82 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 83 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 84 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 85 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 86 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 87 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 88 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 89 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 90 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 91 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 92 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 93 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 94 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 95 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 96 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 97 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 98 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 99 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 100 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 101 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 102 | 1727733 | Pituitary response to growth hormone-releasing hormone in IDDM. |
| 103 | 1727733 | In poorly controlled insulin-dependent diabetes mellitus (IDDM), hyperglycemia fails to inhibit the pituitary response to growth hormone-releasing factor (GRF). |
| 104 | 1727733 | GRF 1-40 was administered to nine poorly controlled IDDM subjects (HbA1 greater than 11.1%) with and without concomitant infusion of insulin. |
| 105 | 1727733 | In the absence of insulin, the poorly controlled IDDM subjects demonstrated a growth hormone response to GRF similar to that of nondiabetic subjects, despite marked hyperglycemia (approximately 16.8 mM). |
| 106 | 1727733 | When insulin was infused into these same patients (insulin clamp) to produce combined hyperinsulinemia (528 +/- 90 pM) and hyperglycemia (16.5 +/- 1.98 mM), the GRF-induced growth hormone rise was markedly exaggerated (65 +/- 11 vs. 20 +/- 4 micrograms/L without insulin infusion, P less than 0.001). |
| 107 | 1727733 | This enhancement of GRF-stimulated growth hormone release by insulin was strikingly attenuated (22 +/- 7 micrograms/L) in five well-controlled diabetic subjects studied under conditions of similar hyperinsulinemia (486 +/- 84 pM) and hyperglycemia (16.41 +/- 0.95 mM). |
| 108 | 1727733 | The paradoxical stimulatory effect of insulin on GRF-induced growth hormone release may contribute to the high spontaneous growth hormone levels characteristically seen in poorly controlled insulin-treated patients, and its attenuation after intensive insulin therapy may contribute to the reversal of growth hormone hypersecretion in well-controlled diabetic patients. |
| 109 | 1759540 | Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in type I diabetic patients. |
| 110 | 1967164 | Altered pituitary growth hormone (GH) regulation in streptozotocin-diabetic rats: a combined defect of hypothalamic somatostatin and GH-releasing factor. |
| 111 | 1967164 | An interplay between hypothalamic GH-releasing factor (GRF) and inhibitory factor [somatostatin (SRIF)] secretion is thought to account for episodic pituitary GH release. |
| 112 | 1967164 | GH synthesis has been shown to be independent of SRIF regulation; however, insulin-like growth factor-I and GRF inhibit and stimulate GH synthesis, respectively. |
| 113 | 1967164 | In diabetic rats insulin-like growth factor-I levels were decreased, appropriate to low GH status, in serum (290 +/- 66 vs. 1662 +/- 92 ng/ml; P less than 0.001) and hypothalamus (6.8 +/- 1.0 vs. 13.0 +/- 0.4 pg/mg wet wt; P less than 0.001) and, thus, did not seem to account for the low AP GH content. |
| 114 | 1967164 | Altered pituitary growth hormone (GH) regulation in streptozotocin-diabetic rats: a combined defect of hypothalamic somatostatin and GH-releasing factor. |
| 115 | 1967164 | An interplay between hypothalamic GH-releasing factor (GRF) and inhibitory factor [somatostatin (SRIF)] secretion is thought to account for episodic pituitary GH release. |
| 116 | 1967164 | GH synthesis has been shown to be independent of SRIF regulation; however, insulin-like growth factor-I and GRF inhibit and stimulate GH synthesis, respectively. |
| 117 | 1967164 | In diabetic rats insulin-like growth factor-I levels were decreased, appropriate to low GH status, in serum (290 +/- 66 vs. 1662 +/- 92 ng/ml; P less than 0.001) and hypothalamus (6.8 +/- 1.0 vs. 13.0 +/- 0.4 pg/mg wet wt; P less than 0.001) and, thus, did not seem to account for the low AP GH content. |
| 118 | 1971774 | The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. |
| 119 | 1971774 | Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. |
| 120 | 1971774 | These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM. |
| 121 | 1971774 | The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. |
| 122 | 1971774 | Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. |
| 123 | 1971774 | These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM. |
| 124 | 1971774 | The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. |
| 125 | 1971774 | Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. |
| 126 | 1971774 | These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM. |
| 127 | 1974524 | [The effect of growth hormone-releasing factor (GRF) on secretion of insulin, glucagon and somatostatin from perfused rat pancreas]. |
| 128 | 1974524 | To examine the effects of growth hormone-releasing factor (GRF) on islet hormone release, rat pancreas was perfused. rhGRF at the concentration of 10(-7) M or more enhanced insulin secretion stimulated by 16.7 mM glucose, hpGRF slightly enhanced insulin secretion as well. |
| 129 | 1974524 | We concluded that rhGRF stimulated insulin, glucagon and somatostatin secretion and the insulin secretion was inhibited by beta-blocker. hpGRF stimulated insulin and glucagon secretion as well. |
| 130 | 1974524 | [The effect of growth hormone-releasing factor (GRF) on secretion of insulin, glucagon and somatostatin from perfused rat pancreas]. |
| 131 | 1974524 | To examine the effects of growth hormone-releasing factor (GRF) on islet hormone release, rat pancreas was perfused. rhGRF at the concentration of 10(-7) M or more enhanced insulin secretion stimulated by 16.7 mM glucose, hpGRF slightly enhanced insulin secretion as well. |
| 132 | 1974524 | We concluded that rhGRF stimulated insulin, glucagon and somatostatin secretion and the insulin secretion was inhibited by beta-blocker. hpGRF stimulated insulin and glucagon secretion as well. |
| 133 | 2110412 | Conflicting data are found in the literature concerning the growth hormone response to growth hormone-releasing hormone and the insulin-like growth factor I level in Type I diabetes mellitus. |
| 134 | 2110412 | The GH response to GHRH and the serum IGF-I level were studied in 29 moderately to well regulated male diabetic patients and 20 age-matched controls. |
| 135 | 2110412 | It is concluded that in Type I diabetes the GH response to GHRH is increased, even in well regulated patients, and that the serum IGF-I level is depressed. |
| 136 | 2110412 | Conflicting data are found in the literature concerning the growth hormone response to growth hormone-releasing hormone and the insulin-like growth factor I level in Type I diabetes mellitus. |
| 137 | 2110412 | The GH response to GHRH and the serum IGF-I level were studied in 29 moderately to well regulated male diabetic patients and 20 age-matched controls. |
| 138 | 2110412 | It is concluded that in Type I diabetes the GH response to GHRH is increased, even in well regulated patients, and that the serum IGF-I level is depressed. |
| 139 | 2110412 | Conflicting data are found in the literature concerning the growth hormone response to growth hormone-releasing hormone and the insulin-like growth factor I level in Type I diabetes mellitus. |
| 140 | 2110412 | The GH response to GHRH and the serum IGF-I level were studied in 29 moderately to well regulated male diabetic patients and 20 age-matched controls. |
| 141 | 2110412 | It is concluded that in Type I diabetes the GH response to GHRH is increased, even in well regulated patients, and that the serum IGF-I level is depressed. |
| 142 | 2172669 | The plasma levels of the following hormones were measured: basal thyroxine (T4), estradiol and cortisol; and also follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and adrenocorticotropic hormone (ACTH), basally and after acute challenge with LH releasing hormone (LHRH), GRF (1-29)NH2 or insulin hypoglycemia, TSH releasing hormone (TRH) and lysine-8-vasopressin, respectively. |
| 143 | 2229305 | In the present study we investigated the effects of the acetylcholinesterase inhibitor pyridostigmine (PD), which is hypothesized to decrease hypothalamic somatostatin tone, alone and in association with GH-releasing hormone (GHRH) on GH secretion in 18 type 1 diabetic patients and 12 normal subjects using a randomized double blind placebo-controlled protocol. |
| 144 | 2465694 | The abilities of human and rat growth hormone-releasing factors (hGHRF, rGHRF), peptide histidine isoleucine or methionine (PHI, PHM) and the Gila monster venom peptides (helospectin I, helospectin II, and helodermin) to interact with guinea pig pancreatic acini were characterized and compared with vasoactive intestinal peptide (VIP) and secretin. |
| 145 | 2465694 | Each peptide inhibited 125I-labeled secretin binding with the potencies: secretin greater than helospectin I = helospectin II = helodermin greater than rGHRF = PHI = VIP greater than PHM greater than hGHRF. |
| 146 | 2465694 | VIP or rGHRF and PHI or PHM demonstrated high and low selectivity, respectively, for VIP receptors, secretin high selectivity for the secretin receptor, and helospectin I or II and helodermin a relatively high affinity for both VIP and secretin receptors. |
| 147 | 2465694 | The abilities of human and rat growth hormone-releasing factors (hGHRF, rGHRF), peptide histidine isoleucine or methionine (PHI, PHM) and the Gila monster venom peptides (helospectin I, helospectin II, and helodermin) to interact with guinea pig pancreatic acini were characterized and compared with vasoactive intestinal peptide (VIP) and secretin. |
| 148 | 2465694 | Each peptide inhibited 125I-labeled secretin binding with the potencies: secretin greater than helospectin I = helospectin II = helodermin greater than rGHRF = PHI = VIP greater than PHM greater than hGHRF. |
| 149 | 2465694 | VIP or rGHRF and PHI or PHM demonstrated high and low selectivity, respectively, for VIP receptors, secretin high selectivity for the secretin receptor, and helospectin I or II and helodermin a relatively high affinity for both VIP and secretin receptors. |
| 150 | 2482123 | We have shown in the companion paper that somatotrophs dispersed from streptozotocin diabetic rats exhibit altered sensitivity to the natural hypothalamic controlling hormones, growth hormone releasing factor and somatostatin. |
| 151 | 2504552 | Growth hormone (GH) secretion is mediated by hypothalamic factors, mainly growth hormone releasing factor (GRF) and somatostatin (SS). |
| 152 | 2537716 | Fifteen of 18 patients with vasoactive intestinal peptide-producing tumors, 8 of 8 patients with glucagonomas, 7 of 7 patients with unresectable insulinomas, and 3 of 3 patients with growth hormone releasing factor-producing tumors had a good sustained symptomatic response to SMS 201-995. |
| 153 | 2575447 | These studies suggest somatotrophs of diabetic rats have altered sensitivity in vitro to the controlling hormones growth hormone releasing factor and somatostatin. |
| 154 | 2753972 | As a group, serum insulin-like growth factor-I was lower in DM vs. non-DM individuals (P = 0.0014), although when separated by sex this difference did not reach statistical significance in women (P = 0.317). |
| 155 | 2753972 | The altered frequency of GH pulses together with enhanced interpulse GH concentrations and an amplified circadian GH rhythm are compatible with hypothalamic dysfunction associated with dysregulation of somatostatin and/or GHRH secretion. |
| 156 | 2868453 | [Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. |
| 157 | 2868453 | A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. |
| 158 | 2868453 | [Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. |
| 159 | 2868453 | A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. |
| 160 | 2874906 | Cholinergic muscarinic blockade did not alter the GH responses to GRF and TRH in patients with acromegaly. |
| 161 | 2881511 | GH secretory bursts are due to the combination of a pulsatile GRF release and a decreased Somatostatin secretion in hypophysial portal blood. |
| 162 | 2888037 | The GH response to 2-min pulses of hGRF at concentrations of 1.56, 6.25, and 25 pM with and without somatostatin 10(-9) M was significantly greater in the diabetic group than in the control group. |
| 163 | 2896808 | Plasma growth hormone-releasing hormone levels in type 1 (insulin-dependent) diabetic children following a mixed meal. |
| 164 | 2896808 | These results indicate that circulating growth hormone-releasing hormone does not play a dominant role in the regulation of insulin and somatostatin. |
| 165 | 2896808 | Plasma growth hormone-releasing hormone levels in type 1 (insulin-dependent) diabetic children following a mixed meal. |
| 166 | 2896808 | These results indicate that circulating growth hormone-releasing hormone does not play a dominant role in the regulation of insulin and somatostatin. |
| 167 | 2901949 | The effects of the diabetic state on the somatotroph's responsiveness to the secretagogues GRF and (Bu)2-cAMP and to the inhibitor somatostatin (SRIF) were evaluated in enzymatically dissociated rat adenohypophyseal cells in primary monolayer culture. |
| 168 | 2916380 | The response to GH releasing hormone (GHRH 1-29) and 24-h serum GH and IGF-I levels were measured in 9 insulin-dependent diabetics with retinopathy and 6 normal volunteers before and after different treatment regimens with octreotide, a long-acting somatostatin analogue. |
| 169 | 2929237 | Comparison of results of insulin-induced hypoglycemia testing and stimulation tests by CRH and GHRH suggested that all patients had a primary suprahypophyseal lesion rather than a primary pituitary defect. |
| 170 | 3070044 | Five mutated genes on chromosome 20 have a relation to disease: a mutation in the adenosine deaminase gene results in a deficiency of the enzyme and severe combined immune deficiency; mutations in the gene for the growth hormone releasing factor result in some forms of dwarfism; mutations in the closely linked genes for the hormones arginine vasopressin and oxytocin and their neurophysins are probably responsible for some diabetes insipidus; and mutations in the gene that regulates both alpha-neuraminidase and beta-galactosidase activities determine galactosialidosis. |
| 171 | 3070044 | Two genes that code for tyrosine kinases are on the chromosome, SRC1 the proto-oncogene and a gene (HCK) coding for haemopoietic kinase (an src-like kinase), but no direct relation to cancer has been shown for either of these kinases. |
| 172 | 3070044 | Twenty-four additional loci are assigned to the chromosome: five genes that code for binding proteins, one for a light chain of ferritin, genes for three enzymes (inosine triphosphatase, s-adenosylhomocysteine hydrolase, and sterol delta 24-reductase), one for each of a secretory protein and an opiate neuropeptide, a cell surface antigen, two fragile sites, and 10 DNA sequences (one satellite and nine unique) that detect RFLPs. |
| 173 | 3082700 | Insulin receptor antiserum blocked the suppression of GH by 7 nM insulin, but had no effect on the suppression of GH by IGF-I (3.25 nM). |
| 174 | 3082700 | Insulin (7 nM) prevented the stimulation of GH induced by up to 1 nM GRF (P less than 0.01) and this suppression was also selectively blocked by insulin receptor antiserum. |
| 175 | 3082700 | The inhibition of GRF-stimulated GH required a lag period of 48 h and the dose of insulin required for 50% inhibition of GRF stimulation was 3.5 nM. |
| 176 | 3082700 | Fibroblast growth factor, epidermal growth factor, and insulin A-chain at similar doses did not alter basal or GRF-stimulated GH secretion. |
| 177 | 3082700 | Insulin receptor antiserum blocked the suppression of GH by 7 nM insulin, but had no effect on the suppression of GH by IGF-I (3.25 nM). |
| 178 | 3082700 | Insulin (7 nM) prevented the stimulation of GH induced by up to 1 nM GRF (P less than 0.01) and this suppression was also selectively blocked by insulin receptor antiserum. |
| 179 | 3082700 | The inhibition of GRF-stimulated GH required a lag period of 48 h and the dose of insulin required for 50% inhibition of GRF stimulation was 3.5 nM. |
| 180 | 3082700 | Fibroblast growth factor, epidermal growth factor, and insulin A-chain at similar doses did not alter basal or GRF-stimulated GH secretion. |
| 181 | 3082700 | Insulin receptor antiserum blocked the suppression of GH by 7 nM insulin, but had no effect on the suppression of GH by IGF-I (3.25 nM). |
| 182 | 3082700 | Insulin (7 nM) prevented the stimulation of GH induced by up to 1 nM GRF (P less than 0.01) and this suppression was also selectively blocked by insulin receptor antiserum. |
| 183 | 3082700 | The inhibition of GRF-stimulated GH required a lag period of 48 h and the dose of insulin required for 50% inhibition of GRF stimulation was 3.5 nM. |
| 184 | 3082700 | Fibroblast growth factor, epidermal growth factor, and insulin A-chain at similar doses did not alter basal or GRF-stimulated GH secretion. |
| 185 | 3098456 | Four of the patients with no GH response during insulin tolerance tests (ITT) showed increased GH in response to synthetic human growth hormone releasing factor (GRF-44). |
| 186 | 3098456 | Prolactin was raised in all seven women and increased further in response to TRH. |
| 187 | 3106123 | Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. |
| 188 | 3106123 | Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. |
| 189 | 3106123 | In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. |
| 190 | 3106123 | Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. |
| 191 | 3106123 | Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. |
| 192 | 3106123 | In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. |
| 193 | 3106123 | Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. |
| 194 | 3106123 | Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. |
| 195 | 3106123 | In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. |
| 196 | 3123283 | In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4 +/- 8.6 pg/ml and 12.2 +/- 1.4 ng/ml and in the low or non responder 14.7 +/- 1.5 pg/ml and 2.0 +/- 0.6 ng/ml, respectively. |
| 197 | 3126122 | We administered growth-hormone releasing hormone (GHRH), clonidine or thyrotropin-releasing hormone (TRH) as intravenous boli each in three different randomized mornings to nine well-controlled Type 1 diabetic men and to six age-matched healthy men who served as controls. |
| 198 | 3132856 | The role that growth hormone (GH), growth hormone releasing factor (GHRF), and insulinlike growth factor-1 (IGF-1) play in these processes has been investigated using transgenic mice chronically expressing these hormones. |
| 199 | 3139333 | We have investigated fasting GH levels and the response to 100 micrograms i.v. growth hormone releasing factor, GRF(1-29)NH2, in age-matched men: six normal weight controls, six obese controls, six insulin-dependent diabetics, six normal weight non-insulin dependent diabetics and six obese non-insulin dependent diabetics. |
| 200 | 3139333 | The peak GH response to GRF was similar in the controls, insulin-dependent diabetics (IDD) and non-insulin dependent (NIDD) normal weight diabetics (mean peak +/- SEM: controls 25.5 +/- 5 mU/l, IDD 26.5 +/- 6 mU/l, NIDD 19.7 +/- 5 mU/l) but was significantly reduced in the two obese groups (obese 6.4 +/- 3 mU/l, obese diabetics 4.5 +/- 1 mU/l, P less than 0.01). |
| 201 | 3139333 | We have investigated fasting GH levels and the response to 100 micrograms i.v. growth hormone releasing factor, GRF(1-29)NH2, in age-matched men: six normal weight controls, six obese controls, six insulin-dependent diabetics, six normal weight non-insulin dependent diabetics and six obese non-insulin dependent diabetics. |
| 202 | 3139333 | The peak GH response to GRF was similar in the controls, insulin-dependent diabetics (IDD) and non-insulin dependent (NIDD) normal weight diabetics (mean peak +/- SEM: controls 25.5 +/- 5 mU/l, IDD 26.5 +/- 6 mU/l, NIDD 19.7 +/- 5 mU/l) but was significantly reduced in the two obese groups (obese 6.4 +/- 3 mU/l, obese diabetics 4.5 +/- 1 mU/l, P less than 0.01). |
| 203 | 3144116 | The GH response to GHRH was not correlated with the GH response to arginine-insulin tolerance test (AITT). |
| 204 | 3751451 | They showed absent growth hormone (GH) response to insulin-hypoglycaemia or glucagon, but responded to 100 micrograms growth hormone releasing factor (GRF-44) with a rise in circulating GH, suggesting a hypothalamic defect in GH release though a co-existing pituitary defect cannot be excluded. |
| 205 | 3877029 | We describe a male infant with septo-optic dysplasia in whom extensive endocrine evaluation revealed central diabetes insipidus, hypothalamic hypothyroidism and combined (hypothalamic-pituitary) hypoadrenalism, along with normal pituitary growth hormone reserve. |
| 206 | 3877029 | This is the first reported case of a patient with septo-optic dysplasia who underwent corticotropin-releasing factor and growth hormone-releasing hormone stimulation. |
| 207 | 3889029 | Since GH induces the production of insulin-like growth factors (IGF) in liver and other tissues, it is of interest to learn whether IGF alters GH release through long loop feedback inhibition. |
| 208 | 3889029 | Binding studies using 125I-labeled IGF-I, IGF-II, and insulin revealed specific hormone binding for each ligand to cell membranes derived from four somatotropinomas. |
| 209 | 3889029 | In a single tumor, insulin also partially inhibited GHRH-stimulated GH release. |
| 210 | 3889029 | Additionally, in one nonadenomatous pituitary removed from a patient with diabetes mellitus, insulin and somatomedin inhibited GHRH-stimulated GH release, and insulin inhibited basal GH secretion. |
| 211 | 3889029 | Since GH induces the production of insulin-like growth factors (IGF) in liver and other tissues, it is of interest to learn whether IGF alters GH release through long loop feedback inhibition. |
| 212 | 3889029 | Binding studies using 125I-labeled IGF-I, IGF-II, and insulin revealed specific hormone binding for each ligand to cell membranes derived from four somatotropinomas. |
| 213 | 3889029 | In a single tumor, insulin also partially inhibited GHRH-stimulated GH release. |
| 214 | 3889029 | Additionally, in one nonadenomatous pituitary removed from a patient with diabetes mellitus, insulin and somatomedin inhibited GHRH-stimulated GH release, and insulin inhibited basal GH secretion. |
| 215 | 3924695 | Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. |
| 216 | 3924695 | Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. |
| 217 | 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. |
| 218 | 3924695 | Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. |
| 219 | 3924695 | Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. |
| 220 | 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. |
| 221 | 6242799 | To assess pituitary and hypothalamic function in diabetes, 100 micrograms growth hormone releasing factor 1-44 was administered to 10 normal subjects at fasting plasma glucose (5.2 +/- 0.1 mmol/l, mean +/- S.E.M.), 10 insulin-dependent diabetics while euglycaemic (6.4 +/- 0.3 mmol/l), and 10 while hyperglycaemic (13.1 +/- 1.3 mmol/l). |
| 222 | 6409361 | The capability of the anterior pituitary to secrete growth hormone in response to an IV injection of somatocrinin (120 micrograms 4 micrograms/kg) was documented, therefore proving the hypothalamic origin of the deficit which had been suspected because of association of diabetes insipidus and hyperprolactinemia. |
| 223 | 6430738 | Furthermore, five additional diabetic subjects with normal growth hormone levels after long-term insulin pump treatment also showed an identical response to GRF. |
| 224 | 6430738 | Thus, raised basal growth hormone levels in diabetes and the fall that follows intensive insulin treatment may reflect changes in hypothalamic regulation of, rather than in pituitary responsiveness to, GRF. |
| 225 | 6430738 | Furthermore, five additional diabetic subjects with normal growth hormone levels after long-term insulin pump treatment also showed an identical response to GRF. |
| 226 | 6430738 | Thus, raised basal growth hormone levels in diabetes and the fall that follows intensive insulin treatment may reflect changes in hypothalamic regulation of, rather than in pituitary responsiveness to, GRF. |
| 227 | 6439589 | Impaired growth hormone response to human pancreatic growth hormone releasing factor [GRF(1-44)] in type 2 (non-insulin-dependent) diabetes. |
| 228 | 6439589 | Human pancreatic growth hormone releasing factor [GRF(1-44)] is the largest molecule of several peptides recently isolated from pancreatic tumours associated with acromegaly. |
| 229 | 6439589 | GRF(1-44) stimulated the release of growth hormone in normal subjects and produced no side effects. |
| 230 | 6439589 | Impaired growth hormone response to human pancreatic growth hormone releasing factor [GRF(1-44)] in type 2 (non-insulin-dependent) diabetes. |
| 231 | 6439589 | Human pancreatic growth hormone releasing factor [GRF(1-44)] is the largest molecule of several peptides recently isolated from pancreatic tumours associated with acromegaly. |
| 232 | 6439589 | GRF(1-44) stimulated the release of growth hormone in normal subjects and produced no side effects. |
| 233 | 6439589 | Impaired growth hormone response to human pancreatic growth hormone releasing factor [GRF(1-44)] in type 2 (non-insulin-dependent) diabetes. |
| 234 | 6439589 | Human pancreatic growth hormone releasing factor [GRF(1-44)] is the largest molecule of several peptides recently isolated from pancreatic tumours associated with acromegaly. |
| 235 | 6439589 | GRF(1-44) stimulated the release of growth hormone in normal subjects and produced no side effects. |
| 236 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 237 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 238 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 239 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 240 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 241 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 242 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 243 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 244 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 245 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 246 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 247 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 248 | 7552296 | Time course of hypothalamic growth hormone-releasing hormone and somatostatin content in streptozocin diabetic rats: evidence for early changes in hypothalamic regulation. |
| 249 | 7552296 | Our studies were designed to delineate early changes in hypothalamic regulation by growth hormone-releasing hormone (GHRH) and somatostatin (SS) with the aim of determining the best time period for hypothalamic secretion studies. |
| 250 | 7552296 | We examined hypothalamic GHRH content and SS concentration in control, diabetic, and insulin treated diabetic rats (n = 5-13; streptozocin 100 mg/kg i.p.) at 0, 2, 4, 7, 10 and 21 days. |
| 251 | 7552296 | GHRH content of insulin treated diabetic rats was elevated at day 2 (158 +/- 10%, P < 0.05), but subsequently was unchanged from control. |
| 252 | 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. |
| 253 | 7554320 | Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. |
| 254 | 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. |
| 255 | 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. |
| 256 | 7554320 | Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. |
| 257 | 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. |
| 258 | 7575177 | The growth promoting actions of growth hormone are indirect and mediated through generations of insulin-like growth factors. |
| 259 | 7575177 | Growth hormone release is determined by a dynamic equilibrium between the inhibitory and stimulatory hypothalamic peptides, somatostatin and growth hormone-releasing hormone. |
| 260 | 7647774 | We have also investigated the role of endogenous somatostatin (SS) and cholinergic manipulation on the GH responses to GH-releasing hormone (GHRH). |
| 261 | 7647774 | Pretreatment of older rats (16 weeks) with anti-somatostatin antibodies (SS-Ab) significantly increased GH responses to GHRH in both normal and GK groups. |
| 262 | 7647774 | We have also investigated the role of endogenous somatostatin (SS) and cholinergic manipulation on the GH responses to GH-releasing hormone (GHRH). |
| 263 | 7647774 | Pretreatment of older rats (16 weeks) with anti-somatostatin antibodies (SS-Ab) significantly increased GH responses to GHRH in both normal and GK groups. |
| 264 | 7674023 | Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. |
| 265 | 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. |
| 266 | 7674023 | Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone-releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland. |
| 267 | 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. |
| 268 | 7729789 | Blunted GH response to growth hormone-releasing hormone (GHRH) alone or combined with arginine in non-insulin-dependent diabetes mellitus. |
| 269 | 7729789 | In 14 patients with NIDDM, 7 normal weight (NWD) and 7 obese (OD), we investigated the somatotrope responsiveness to GHRH (1 microgram/kg) alone or combined with arginine (ARG, 0.5 g/kg), which is able to enhance the GH response to GHRH, probably by inhibiting somatostatin release from hypothalamus. |
| 270 | 7729789 | GH but not IGF-I levels were higher (p < 0.05) in NS than in OP (1.5 +/- 0.5 vs 0.5 +/- 0.2 microgram/l). |
| 271 | 7729789 | Blunted GH response to growth hormone-releasing hormone (GHRH) alone or combined with arginine in non-insulin-dependent diabetes mellitus. |
| 272 | 7729789 | In 14 patients with NIDDM, 7 normal weight (NWD) and 7 obese (OD), we investigated the somatotrope responsiveness to GHRH (1 microgram/kg) alone or combined with arginine (ARG, 0.5 g/kg), which is able to enhance the GH response to GHRH, probably by inhibiting somatostatin release from hypothalamus. |
| 273 | 7729789 | GH but not IGF-I levels were higher (p < 0.05) in NS than in OP (1.5 +/- 0.5 vs 0.5 +/- 0.2 microgram/l). |
| 274 | 7798026 | The number of GH-releasing factor (GRF)-labelled axons and the amount of axonal tyrosine hydroxylase (TH)-immunoreactivity increased in STZ-D. |
| 275 | 7798026 | There were no significant differences in any of the other densitometrical measurements performed on GRF-, somatostatin-, thyrotropin-releasing hormone- and TH-labelled ME axon cross-sections as well as those on tuberoinfundibular-dopaminergic neurones of the AN in STZ-D compared with control rats. |
| 276 | 7798026 | The number of GH-releasing factor (GRF)-labelled axons and the amount of axonal tyrosine hydroxylase (TH)-immunoreactivity increased in STZ-D. |
| 277 | 7798026 | There were no significant differences in any of the other densitometrical measurements performed on GRF-, somatostatin-, thyrotropin-releasing hormone- and TH-labelled ME axon cross-sections as well as those on tuberoinfundibular-dopaminergic neurones of the AN in STZ-D compared with control rats. |
| 278 | 8028515 | Pyridostigmine (PD), an acetylcholinesterase inhibitor, elicits GH secretion when administered alone and enhances the GH response to GHRH in normal subjects. |
| 279 | 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. |
| 280 | 8258646 | Pyridostigmine (PD), an acetylcholinesterase inhibitor, has been shown to reduce the variability of the GH response to GHRH in normal subjects. |
| 281 | 8325951 | GH hypersecretion in insulin-dependent diabetes (IDDM) is well documented. |
| 282 | 8325951 | The 24-h GH and blood glucose profiles, insulin-like growth factor I (IGF-I) concentrations and GH responses to GRF were analyzed in 21 insulin-dependent diabetics and 4 healthy subjects before and after 7 days treatment with recombinant human GH (rhGH) (4 IU given sc at 0800 h). |
| 283 | 8325951 | According to C-peptide response to glucagon IDDM patients were subdivided into C-peptide negative (CpN, n = 12) patients without endogenous pancreatic beta-cell activity and C-peptide positive (CpP, (n = 9) patients with endogenous insulin secretion. |
| 284 | 8325951 | The response of GH to GRF in CpN diabetics was however, almost unchanged after treatment whereas it became lower in CpP diabetics and controls. |
| 285 | 8325951 | The dose of 4 IU of rhGH increased significantly GH levels in diabetics with preserved beta-cell function with consequent increase in IGF-I levels and attenuation of GRF induced GH response. |
| 286 | 8325951 | In addition, neither increase in IGF-I levels nor suppression of GH response to GRF on rhGH treatment was observed in CpN diabetics. |
| 287 | 8325951 | The results are in keeping with an important role of portal insulin in GH-induced hepatic IGF-I secretion. |
| 288 | 8325951 | GH hypersecretion in insulin-dependent diabetes (IDDM) is well documented. |
| 289 | 8325951 | The 24-h GH and blood glucose profiles, insulin-like growth factor I (IGF-I) concentrations and GH responses to GRF were analyzed in 21 insulin-dependent diabetics and 4 healthy subjects before and after 7 days treatment with recombinant human GH (rhGH) (4 IU given sc at 0800 h). |
| 290 | 8325951 | According to C-peptide response to glucagon IDDM patients were subdivided into C-peptide negative (CpN, n = 12) patients without endogenous pancreatic beta-cell activity and C-peptide positive (CpP, (n = 9) patients with endogenous insulin secretion. |
| 291 | 8325951 | The response of GH to GRF in CpN diabetics was however, almost unchanged after treatment whereas it became lower in CpP diabetics and controls. |
| 292 | 8325951 | The dose of 4 IU of rhGH increased significantly GH levels in diabetics with preserved beta-cell function with consequent increase in IGF-I levels and attenuation of GRF induced GH response. |
| 293 | 8325951 | In addition, neither increase in IGF-I levels nor suppression of GH response to GRF on rhGH treatment was observed in CpN diabetics. |
| 294 | 8325951 | The results are in keeping with an important role of portal insulin in GH-induced hepatic IGF-I secretion. |
| 295 | 8325951 | GH hypersecretion in insulin-dependent diabetes (IDDM) is well documented. |
| 296 | 8325951 | The 24-h GH and blood glucose profiles, insulin-like growth factor I (IGF-I) concentrations and GH responses to GRF were analyzed in 21 insulin-dependent diabetics and 4 healthy subjects before and after 7 days treatment with recombinant human GH (rhGH) (4 IU given sc at 0800 h). |
| 297 | 8325951 | According to C-peptide response to glucagon IDDM patients were subdivided into C-peptide negative (CpN, n = 12) patients without endogenous pancreatic beta-cell activity and C-peptide positive (CpP, (n = 9) patients with endogenous insulin secretion. |
| 298 | 8325951 | The response of GH to GRF in CpN diabetics was however, almost unchanged after treatment whereas it became lower in CpP diabetics and controls. |
| 299 | 8325951 | The dose of 4 IU of rhGH increased significantly GH levels in diabetics with preserved beta-cell function with consequent increase in IGF-I levels and attenuation of GRF induced GH response. |
| 300 | 8325951 | In addition, neither increase in IGF-I levels nor suppression of GH response to GRF on rhGH treatment was observed in CpN diabetics. |
| 301 | 8325951 | The results are in keeping with an important role of portal insulin in GH-induced hepatic IGF-I secretion. |
| 302 | 8325951 | GH hypersecretion in insulin-dependent diabetes (IDDM) is well documented. |
| 303 | 8325951 | The 24-h GH and blood glucose profiles, insulin-like growth factor I (IGF-I) concentrations and GH responses to GRF were analyzed in 21 insulin-dependent diabetics and 4 healthy subjects before and after 7 days treatment with recombinant human GH (rhGH) (4 IU given sc at 0800 h). |
| 304 | 8325951 | According to C-peptide response to glucagon IDDM patients were subdivided into C-peptide negative (CpN, n = 12) patients without endogenous pancreatic beta-cell activity and C-peptide positive (CpP, (n = 9) patients with endogenous insulin secretion. |
| 305 | 8325951 | The response of GH to GRF in CpN diabetics was however, almost unchanged after treatment whereas it became lower in CpP diabetics and controls. |
| 306 | 8325951 | The dose of 4 IU of rhGH increased significantly GH levels in diabetics with preserved beta-cell function with consequent increase in IGF-I levels and attenuation of GRF induced GH response. |
| 307 | 8325951 | In addition, neither increase in IGF-I levels nor suppression of GH response to GRF on rhGH treatment was observed in CpN diabetics. |
| 308 | 8325951 | The results are in keeping with an important role of portal insulin in GH-induced hepatic IGF-I secretion. |
| 309 | 8580571 | Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. |
| 310 | 8580571 | Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. |
| 311 | 8586028 | Secretion of growth hormone (GH) is excessive in acromegaly, but also in a number of other pathological states such as anorexia nervosa, insulin-dependent diabetes mellitus (IDDM), liver cirrhosis, depression, renal failure and GH-insensitivity syndrome. |
| 312 | 8586028 | In the cohort of brain neurotransmitters, catecholamines and acetylcholine reportedly play a major role in the control of neurosecretory GH-releasing hormone (GHRH) and somatostatin (SS)-producing neurons, and hence GH secretion. |
| 313 | 8699131 | GRF mRNA was significantly (P < 0.001) decreased in the hypothalamus of STZ-diabetic rats (0.2 +/- 0.07 mean relative densitometric units, n = 8) compared with controls (1.0 +/- 0.19, n = 8) with no change in somatostatin mRNA expression. |
| 314 | 8699131 | Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1.1 +/- 0.17, n = 5) with no effect on testicular GRF mRNA expression. |
| 315 | 8699131 | While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. |
| 316 | 8699131 | GRF mRNA was significantly (P < 0.001) decreased in the hypothalamus of STZ-diabetic rats (0.2 +/- 0.07 mean relative densitometric units, n = 8) compared with controls (1.0 +/- 0.19, n = 8) with no change in somatostatin mRNA expression. |
| 317 | 8699131 | Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1.1 +/- 0.17, n = 5) with no effect on testicular GRF mRNA expression. |
| 318 | 8699131 | While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. |
| 319 | 8699131 | GRF mRNA was significantly (P < 0.001) decreased in the hypothalamus of STZ-diabetic rats (0.2 +/- 0.07 mean relative densitometric units, n = 8) compared with controls (1.0 +/- 0.19, n = 8) with no change in somatostatin mRNA expression. |
| 320 | 8699131 | Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1.1 +/- 0.17, n = 5) with no effect on testicular GRF mRNA expression. |
| 321 | 8699131 | While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. |
| 322 | 8723046 | Laboratory examination showed hyperglycemia, increased glycosilated hemoglobin (HbA1c) and insulin resistance on euglycemic glucose clamp. |
| 323 | 8723046 | Blunted growth hormone (GH) secretion was shown in response to insulin-induced hypoglycemia, arginine infusion, and GH-releasing hormone (GHRH) loading test, and in 24 h spontaneous GH profile. |
| 324 | 8740200 | The attenuated inhibitory action of octreotide, a somatostatin analogue on GHRH-induced growth hormone response in type I diabetes mellitus. |
| 325 | 8740245 | Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients. |
| 326 | 8740245 | In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). |
| 327 | 8740245 | Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. |
| 328 | 8740245 | We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. |
| 329 | 8740245 | The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained. |
| 330 | 8740245 | Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients. |
| 331 | 8740245 | In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). |
| 332 | 8740245 | Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. |
| 333 | 8740245 | We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. |
| 334 | 8740245 | The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained. |
| 335 | 8740245 | Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients. |
| 336 | 8740245 | In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). |
| 337 | 8740245 | Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. |
| 338 | 8740245 | We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. |
| 339 | 8740245 | The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained. |
| 340 | 8740245 | Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients. |
| 341 | 8740245 | In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). |
| 342 | 8740245 | Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. |
| 343 | 8740245 | We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. |
| 344 | 8740245 | The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained. |
| 345 | 8740245 | Effect of growth hormone releasing hormone on growth hormone, prostaglandin E2 and insulin in non-insulin-dependent diabetic patients. |
| 346 | 8740245 | In the present study the response of GH, PGE2 and insulin to GHRH (1 microgram/kg b.w.) intravenously was investigated in 12 poorly controlled non-insulin-dependent diabetic patients (8 males and 4 females) and 10 normal volunteers (5 males and 5 females). |
| 347 | 8740245 | Serum insulin decreased significantly after GHRH in both normal subjects and diabetic patients at 60 min. |
| 348 | 8740245 | We conclude that GH response to GHRH is not significantly impaired in poorly controlled non-insulin-dependent diabetic patients. |
| 349 | 8740245 | The physiological significance of the GHRH suppressive effect on serum insulin remains to be explained. |
| 350 | 8799695 | We hypothesize that a reduction in the hypothalamic somatostatin inhibitory tone combined with increased pituitary GH production may be responsible for the pattern of the GH responses to hexarelin and GHRH observed in our type I diabetic patients. |
| 351 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 352 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 353 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 354 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 355 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 356 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 357 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 358 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 359 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 360 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 361 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 362 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 363 | 8943764 | Desensitisation of somatostatin, TRH and GHRH responses to glucose in the diabetic (Goto-Kakizaki) rat hypothalamus. |
| 364 | 8943764 | We have studied the effects of glucose on the release of somatostatin (SS), TRH and GHRH from incubated hypothalami of normal and genetically diabetic, Goto-Kakizaki (GK) rats. |
| 365 | 8943764 | The active isomer D-glucose caused a dose-related inhibition of SS, TRH and GHRH from normal rat hypothalami over a 20-min incubation period in vitro. |
| 366 | 8943764 | These data indicate that the sensitivity of SS-, TRH- and GHRH-producing hypothalamic neurones is reduced in diabetic rats. |
| 367 | 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. |
| 368 | 9063651 | Plasma samples were assayed for adrenocorticotropin (ACTH), cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. |
| 369 | 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. |
| 370 | 9063651 | At 2 and 10 wk after hypophysectomy, there were no responses of plasma GH, LH, PRL, and alpha-MSH to stimulation. |
| 371 | 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. |
| 372 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 373 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 374 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 375 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 376 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 377 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 378 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 379 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 380 | 9109840 | Insulin-dependent (type I) diabetic patients are known to have an exaggerated growth hormone (GH) response to GH-releasing hormone (GHRH), which is hypothesized to be due to a decrease in somatostatin tone. |
| 381 | 9109840 | The aim of the study was to ascertain the influence of the presence and activity of the autoimmune process involving a key enzyme (glutamic acid decarboxylase [GAD]) in the synthetic pathway of a neurotransmitter regulating somatostatin secretion, ie, gamma-aminobutyric acid (GABA), on the GH response to GHRH alone or combined with an acetylcholinesterase inhibitor, pyridostigmine (PD), in patients with type I diabetes mellitus. |
| 382 | 9109840 | Diabetic subjects with serum GAD antibody (GADA) levels more than 3 U (n = 10) showed significantly higher serum GH levels after GHRH injection as compared both with diabetic patients with GADA less than 3 U (n = 10) and with normal controls, whether expressed as absolute or peak values. |
| 383 | 9109840 | The mechanism underlying this effect is hypothesized to be the production of antibodies to GAD, a key enzyme in the synthesis of GABA, and in turn a reduced GABAergic stimulatory tone on somatostatin production at the hypothalamic level. |
| 384 | 9178028 | Repeated administration of growth hormone-releasing hormone with or without previous administration of pyridostigmine in insulin-dependent diabetes mellitus. |
| 385 | 9178028 | Since the GH-releasing effect of PD is likely to be mediated by the inhibition of hypothalamic somatostatin release, our results suggest that there is also an impaired somatostatin tone in hyperglycemic type 1 diabetic patients with normal GH response to GHRH. |
| 386 | 9178028 | Repeated administration of growth hormone-releasing hormone with or without previous administration of pyridostigmine in insulin-dependent diabetes mellitus. |
| 387 | 9178028 | Since the GH-releasing effect of PD is likely to be mediated by the inhibition of hypothalamic somatostatin release, our results suggest that there is also an impaired somatostatin tone in hyperglycemic type 1 diabetic patients with normal GH response to GHRH. |
| 388 | 9186309 | In insulin-dependent diabetes mellitus (IDDM), inappropriate growth hormone (GH) responses to several stimuli, including GH-releasing hormone (GHRH), have been described. |
| 389 | 9186309 | The aim of this study was to evaluate whether there is a differential effect of IDDM on GHRP-6- and GHRH-induced GH secretion. |
| 390 | 9186309 | In summary, the effectiveness of GHRP-6 in IDDM could reinforce the evidence that this peptide probably does not release GH through a decrease in hypothalamic somatostatin secretion. |
| 391 | 9186309 | Moreover, our data suggest that both GHRH and GHRP-6 releasing mechanisms are unaltered in IDDM. |
| 392 | 9186309 | In insulin-dependent diabetes mellitus (IDDM), inappropriate growth hormone (GH) responses to several stimuli, including GH-releasing hormone (GHRH), have been described. |
| 393 | 9186309 | The aim of this study was to evaluate whether there is a differential effect of IDDM on GHRP-6- and GHRH-induced GH secretion. |
| 394 | 9186309 | In summary, the effectiveness of GHRP-6 in IDDM could reinforce the evidence that this peptide probably does not release GH through a decrease in hypothalamic somatostatin secretion. |
| 395 | 9186309 | Moreover, our data suggest that both GHRH and GHRP-6 releasing mechanisms are unaltered in IDDM. |
| 396 | 9186309 | In insulin-dependent diabetes mellitus (IDDM), inappropriate growth hormone (GH) responses to several stimuli, including GH-releasing hormone (GHRH), have been described. |
| 397 | 9186309 | The aim of this study was to evaluate whether there is a differential effect of IDDM on GHRP-6- and GHRH-induced GH secretion. |
| 398 | 9186309 | In summary, the effectiveness of GHRP-6 in IDDM could reinforce the evidence that this peptide probably does not release GH through a decrease in hypothalamic somatostatin secretion. |
| 399 | 9186309 | Moreover, our data suggest that both GHRH and GHRP-6 releasing mechanisms are unaltered in IDDM. |
| 400 | 9253362 | A 52-yr-old woman presented with loss of visual acuity, diabetes insipidus, and acromegaly caused by a GHRH-producing endocrine carcinoma metastasized to the pituitary. |
| 401 | 9253362 | The serum GHRH, GH, and insulin-like growth factor I levels of the patient were elevated. |
| 402 | 9253362 | In situ hybridization documented strong signals for GH mRNA and pituitary-specific transcriptional factor Pit-1 mRNA in the hyperplastic somatotrophs. |
| 403 | 9253362 | A weak signal for GHRH receptor mRNA was detected in these somatotrophs. |
| 404 | 9253362 | However, using in situ RT-PCR, GHRH receptor mRNA was more conclusively observed in most of the somatotrophs. |
| 405 | 9253362 | The excessive production of GHRH by metastatic tumor may have resulted in somatotroph hyperplasia by the synergistic effects of Pit-1 and GHRH receptor. |
| 406 | 9253362 | A 52-yr-old woman presented with loss of visual acuity, diabetes insipidus, and acromegaly caused by a GHRH-producing endocrine carcinoma metastasized to the pituitary. |
| 407 | 9253362 | The serum GHRH, GH, and insulin-like growth factor I levels of the patient were elevated. |
| 408 | 9253362 | In situ hybridization documented strong signals for GH mRNA and pituitary-specific transcriptional factor Pit-1 mRNA in the hyperplastic somatotrophs. |
| 409 | 9253362 | A weak signal for GHRH receptor mRNA was detected in these somatotrophs. |
| 410 | 9253362 | However, using in situ RT-PCR, GHRH receptor mRNA was more conclusively observed in most of the somatotrophs. |
| 411 | 9253362 | The excessive production of GHRH by metastatic tumor may have resulted in somatotroph hyperplasia by the synergistic effects of Pit-1 and GHRH receptor. |
| 412 | 9253362 | A 52-yr-old woman presented with loss of visual acuity, diabetes insipidus, and acromegaly caused by a GHRH-producing endocrine carcinoma metastasized to the pituitary. |
| 413 | 9253362 | The serum GHRH, GH, and insulin-like growth factor I levels of the patient were elevated. |
| 414 | 9253362 | In situ hybridization documented strong signals for GH mRNA and pituitary-specific transcriptional factor Pit-1 mRNA in the hyperplastic somatotrophs. |
| 415 | 9253362 | A weak signal for GHRH receptor mRNA was detected in these somatotrophs. |
| 416 | 9253362 | However, using in situ RT-PCR, GHRH receptor mRNA was more conclusively observed in most of the somatotrophs. |
| 417 | 9253362 | The excessive production of GHRH by metastatic tumor may have resulted in somatotroph hyperplasia by the synergistic effects of Pit-1 and GHRH receptor. |
| 418 | 9253362 | A 52-yr-old woman presented with loss of visual acuity, diabetes insipidus, and acromegaly caused by a GHRH-producing endocrine carcinoma metastasized to the pituitary. |
| 419 | 9253362 | The serum GHRH, GH, and insulin-like growth factor I levels of the patient were elevated. |
| 420 | 9253362 | In situ hybridization documented strong signals for GH mRNA and pituitary-specific transcriptional factor Pit-1 mRNA in the hyperplastic somatotrophs. |
| 421 | 9253362 | A weak signal for GHRH receptor mRNA was detected in these somatotrophs. |
| 422 | 9253362 | However, using in situ RT-PCR, GHRH receptor mRNA was more conclusively observed in most of the somatotrophs. |
| 423 | 9253362 | The excessive production of GHRH by metastatic tumor may have resulted in somatotroph hyperplasia by the synergistic effects of Pit-1 and GHRH receptor. |
| 424 | 9253362 | A 52-yr-old woman presented with loss of visual acuity, diabetes insipidus, and acromegaly caused by a GHRH-producing endocrine carcinoma metastasized to the pituitary. |
| 425 | 9253362 | The serum GHRH, GH, and insulin-like growth factor I levels of the patient were elevated. |
| 426 | 9253362 | In situ hybridization documented strong signals for GH mRNA and pituitary-specific transcriptional factor Pit-1 mRNA in the hyperplastic somatotrophs. |
| 427 | 9253362 | A weak signal for GHRH receptor mRNA was detected in these somatotrophs. |
| 428 | 9253362 | However, using in situ RT-PCR, GHRH receptor mRNA was more conclusively observed in most of the somatotrophs. |
| 429 | 9253362 | The excessive production of GHRH by metastatic tumor may have resulted in somatotroph hyperplasia by the synergistic effects of Pit-1 and GHRH receptor. |
| 430 | 9361690 | To investigate the influence of cholinergic pathways on somatostatin (SS) tone in type I diabetes mellitus, we studied the effect of the muscarinic receptor antagonist pirenzepine ([PZP] 100 mg orally) on spontaneous nocturnal growth hormone (GH) and thyrotropin (TSH) secretion and on their response to GH-releasing hormone (GHRH) in the morning in a group of nine insulin-dependent diabetic patients with poor diabetic control. |
| 431 | 9361690 | The inhibitory effect of PZP on GHRH-induced GH secretion may help to predict nocturnal GH behavior following administration of the drug. |
| 432 | 9361690 | To investigate the influence of cholinergic pathways on somatostatin (SS) tone in type I diabetes mellitus, we studied the effect of the muscarinic receptor antagonist pirenzepine ([PZP] 100 mg orally) on spontaneous nocturnal growth hormone (GH) and thyrotropin (TSH) secretion and on their response to GH-releasing hormone (GHRH) in the morning in a group of nine insulin-dependent diabetic patients with poor diabetic control. |
| 433 | 9361690 | The inhibitory effect of PZP on GHRH-induced GH secretion may help to predict nocturnal GH behavior following administration of the drug. |
| 434 | 9364340 | Growth hormone (GH) secretion is controlled via somatostatin and growth hormone releasing hormone (GHRH). |
| 435 | 9401553 | GHRPs offer the advantage over GHRH in natural models of deranged GH secretion in that, in various metabolic states (e.g. obesity, anorexia nervosa and non-insulin-dependent diabetes mellitus), the GH response to GHRH is more impaired than it is to GHRPs. |
| 436 | 9447286 | Prior to adrenalectomy, TSH, GH or LH showed a low response to TRH, GHRH or LHRH, respectively. |
| 437 | 9524732 | Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2. |
| 438 | 9524732 | Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. |
| 439 | 9524732 | At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3. |
| 440 | 9524732 | Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. |
| 441 | 9524732 | Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2. |
| 442 | 9524732 | Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. |
| 443 | 9524732 | At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3. |
| 444 | 9524732 | Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. |
| 445 | 9524732 | Regulation of pulsatile secretion of growth hormone (GH) relies on hypothalamic neuronal loops, major transmitters involved in their operation are growth hormone releasing hormone (GHRH) synthetized mostly in arcuate nucleus (ARC) neurons, and somatostatin (SRIH), synthetized both in hypothalamus periventricular (PVe) and ARC neurons. 2. |
| 446 | 9524732 | Other neuropeptides synthetized in ARC neurons, such as galanin, or in ARC interneurons, such as neuropeptide Y (NPY), are able to modulate synthesis and release of GHRH and SRIH into the hypothalamohypophyseal portal system. 3. |
| 447 | 9524732 | At the pituitary level, major neurotransmitters regulating GH cells act on receptors of the VIP/PACAP/GHRH family and of the somatostatin family, in particular, sst2 and sst3. |
| 448 | 9524732 | Regulation and differentiation of somatotropes also depend upon paracrine processes within the pituitary itself and involve growth factors and several neuropeptides, for instance, vasoactive intestinal peptide, angiotensin 2, endothelin, and activin. 10. |
| 449 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 450 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 451 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 452 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 453 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 454 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 455 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 456 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 457 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 458 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 459 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 460 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 461 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 462 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 463 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 464 | 9579239 | Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. |
| 465 | 9579239 | Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. |
| 466 | 9579239 | Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. |
| 467 | 9579239 | In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. |
| 468 | 9579239 | These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide. |
| 469 | 9710361 | Molecular cloning of pit-1 cDNA from porcine anterior pituitary and its involvement in pituitary stimulation by growth hormone-releasing factor. |
| 470 | 9710361 | Pit-1/GHF-1 (hereafter Pit-1) is a pituitary-specific transcription factor that participates in growth hormone (GH), prolactin and thyroid-stimulating hormone gene expression and in proliferation of the cells that produce these hormones. |
| 471 | 9710361 | In this study, we determined the nucleotide sequence of porcine Pit-1 cDNA, which shows high homology (95%) with the known mammalian Pit-1s. |
| 472 | 9710361 | The levels of Pit-1, GH, cJun and cFos mRNAs were examined using the reverse transcription-polymerase chain reaction. |
| 473 | 9710361 | Stimulation with GRF for 2 h increased the Pit-1 mRNA level 3-fold. |
| 474 | 9710361 | The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. |
| 475 | 9710361 | These results suggest that increasing Pit-1 mRNA level in response to GRF plays a role in the early event of the GH gene expression or with the assistance of other transcription factors that modulate GH gene. |
| 476 | 9710361 | Molecular cloning of pit-1 cDNA from porcine anterior pituitary and its involvement in pituitary stimulation by growth hormone-releasing factor. |
| 477 | 9710361 | Pit-1/GHF-1 (hereafter Pit-1) is a pituitary-specific transcription factor that participates in growth hormone (GH), prolactin and thyroid-stimulating hormone gene expression and in proliferation of the cells that produce these hormones. |
| 478 | 9710361 | In this study, we determined the nucleotide sequence of porcine Pit-1 cDNA, which shows high homology (95%) with the known mammalian Pit-1s. |
| 479 | 9710361 | The levels of Pit-1, GH, cJun and cFos mRNAs were examined using the reverse transcription-polymerase chain reaction. |
| 480 | 9710361 | Stimulation with GRF for 2 h increased the Pit-1 mRNA level 3-fold. |
| 481 | 9710361 | The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. |
| 482 | 9710361 | These results suggest that increasing Pit-1 mRNA level in response to GRF plays a role in the early event of the GH gene expression or with the assistance of other transcription factors that modulate GH gene. |
| 483 | 9710361 | Molecular cloning of pit-1 cDNA from porcine anterior pituitary and its involvement in pituitary stimulation by growth hormone-releasing factor. |
| 484 | 9710361 | Pit-1/GHF-1 (hereafter Pit-1) is a pituitary-specific transcription factor that participates in growth hormone (GH), prolactin and thyroid-stimulating hormone gene expression and in proliferation of the cells that produce these hormones. |
| 485 | 9710361 | In this study, we determined the nucleotide sequence of porcine Pit-1 cDNA, which shows high homology (95%) with the known mammalian Pit-1s. |
| 486 | 9710361 | The levels of Pit-1, GH, cJun and cFos mRNAs were examined using the reverse transcription-polymerase chain reaction. |
| 487 | 9710361 | Stimulation with GRF for 2 h increased the Pit-1 mRNA level 3-fold. |
| 488 | 9710361 | The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. |
| 489 | 9710361 | These results suggest that increasing Pit-1 mRNA level in response to GRF plays a role in the early event of the GH gene expression or with the assistance of other transcription factors that modulate GH gene. |
| 490 | 9710361 | Molecular cloning of pit-1 cDNA from porcine anterior pituitary and its involvement in pituitary stimulation by growth hormone-releasing factor. |
| 491 | 9710361 | Pit-1/GHF-1 (hereafter Pit-1) is a pituitary-specific transcription factor that participates in growth hormone (GH), prolactin and thyroid-stimulating hormone gene expression and in proliferation of the cells that produce these hormones. |
| 492 | 9710361 | In this study, we determined the nucleotide sequence of porcine Pit-1 cDNA, which shows high homology (95%) with the known mammalian Pit-1s. |
| 493 | 9710361 | The levels of Pit-1, GH, cJun and cFos mRNAs were examined using the reverse transcription-polymerase chain reaction. |
| 494 | 9710361 | Stimulation with GRF for 2 h increased the Pit-1 mRNA level 3-fold. |
| 495 | 9710361 | The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. |
| 496 | 9710361 | These results suggest that increasing Pit-1 mRNA level in response to GRF plays a role in the early event of the GH gene expression or with the assistance of other transcription factors that modulate GH gene. |
| 497 | 9930632 | Growth hormone-insulin-like growth factor-I axis in adult insulin-dependent diabetic patients: evidence for central hypersensitivity to growth hormone-releasing hormone and peripheral resistance to growth hormone. |
| 498 | 9930632 | The aim of this study was to assess the GH-IGFI axis, GH receptor availability, as reflected by the levels of GH-BP, and the amount of GH-dependent IGFBP-3 in adult IDDM patients with different degrees of metabolic control. |
| 499 | 9930632 | Thus, 10 adult well-controlled IDDMs (HbA1 7.8 +/- 0.4%), 10 adult non-ketotic poorly controlled IDDMs (HbA1 13.3 +/- 7%) and 14 sex- and age-matched healthy controls were subjected to two intravenous GH-RH stimulation tests with 0.1 and 1.0 microg/kg body weight respectively, and a plasma IGF-1 generation test induced by the administration of hGH. |
| 500 | 9930632 | Poorly controlled IDDM patients exhibited an exaggerated GH response to 1.0 microg/kg of GH-RH when compared to healthy control subjects. |
| 501 | 9930632 | Low fasting plasma IGF-1 levels and a blunted IGF-1 response to exogenously administered hGH were also found in poorly controlled IDDMs when compared to the healthy control group. |
| 502 | 9930632 | GH-BP levels were significantly lower in IDDMs than in normal controls, and correlated positively with the IGF-1 generation capacity after hGH. |
| 503 | 9930632 | Serum IGFBP-3 levels measured by RIA were similar in IDDM and control groups. |
| 504 | 9930632 | Our findings suggest that IDDM is associated with a diminished availability of GH receptors and synthesis of IGF-1. |
| 505 | 9930632 | Growth hormone-insulin-like growth factor-I axis in adult insulin-dependent diabetic patients: evidence for central hypersensitivity to growth hormone-releasing hormone and peripheral resistance to growth hormone. |
| 506 | 9930632 | The aim of this study was to assess the GH-IGFI axis, GH receptor availability, as reflected by the levels of GH-BP, and the amount of GH-dependent IGFBP-3 in adult IDDM patients with different degrees of metabolic control. |
| 507 | 9930632 | Thus, 10 adult well-controlled IDDMs (HbA1 7.8 +/- 0.4%), 10 adult non-ketotic poorly controlled IDDMs (HbA1 13.3 +/- 7%) and 14 sex- and age-matched healthy controls were subjected to two intravenous GH-RH stimulation tests with 0.1 and 1.0 microg/kg body weight respectively, and a plasma IGF-1 generation test induced by the administration of hGH. |
| 508 | 9930632 | Poorly controlled IDDM patients exhibited an exaggerated GH response to 1.0 microg/kg of GH-RH when compared to healthy control subjects. |
| 509 | 9930632 | Low fasting plasma IGF-1 levels and a blunted IGF-1 response to exogenously administered hGH were also found in poorly controlled IDDMs when compared to the healthy control group. |
| 510 | 9930632 | GH-BP levels were significantly lower in IDDMs than in normal controls, and correlated positively with the IGF-1 generation capacity after hGH. |
| 511 | 9930632 | Serum IGFBP-3 levels measured by RIA were similar in IDDM and control groups. |
| 512 | 9930632 | Our findings suggest that IDDM is associated with a diminished availability of GH receptors and synthesis of IGF-1. |
| 513 | 9930632 | Growth hormone-insulin-like growth factor-I axis in adult insulin-dependent diabetic patients: evidence for central hypersensitivity to growth hormone-releasing hormone and peripheral resistance to growth hormone. |
| 514 | 9930632 | The aim of this study was to assess the GH-IGFI axis, GH receptor availability, as reflected by the levels of GH-BP, and the amount of GH-dependent IGFBP-3 in adult IDDM patients with different degrees of metabolic control. |
| 515 | 9930632 | Thus, 10 adult well-controlled IDDMs (HbA1 7.8 +/- 0.4%), 10 adult non-ketotic poorly controlled IDDMs (HbA1 13.3 +/- 7%) and 14 sex- and age-matched healthy controls were subjected to two intravenous GH-RH stimulation tests with 0.1 and 1.0 microg/kg body weight respectively, and a plasma IGF-1 generation test induced by the administration of hGH. |
| 516 | 9930632 | Poorly controlled IDDM patients exhibited an exaggerated GH response to 1.0 microg/kg of GH-RH when compared to healthy control subjects. |
| 517 | 9930632 | Low fasting plasma IGF-1 levels and a blunted IGF-1 response to exogenously administered hGH were also found in poorly controlled IDDMs when compared to the healthy control group. |
| 518 | 9930632 | GH-BP levels were significantly lower in IDDMs than in normal controls, and correlated positively with the IGF-1 generation capacity after hGH. |
| 519 | 9930632 | Serum IGFBP-3 levels measured by RIA were similar in IDDM and control groups. |
| 520 | 9930632 | Our findings suggest that IDDM is associated with a diminished availability of GH receptors and synthesis of IGF-1. |
| 521 | 10206449 | The growth hormone (GH) response to GH-releasing hormone (GHRH) in patients with non-insulin-dependent diabetes mellitus (NIDDM) was found to be either decreased or normal. |
| 522 | 10372687 | To investigate whether the severity of GHD was correlated with the degree of bone mass and turnover impairment, we evaluated BMD at the lumbar spine and femoral neck; circulating insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and osteocalcin levels, and urinary cross-linked N-telopeptides of type I collagen (Ntx) levels in 101 adult hypopituitary patients and 35 sex- and age-matched healthy subjects. |
| 523 | 10372687 | On the basis of the GH response to arginine plus GHRH (ARG+/-GHRH), patients were subdivided into 4 groups: group 1 included 41 patients with a GH peak below 3 microg/L (0.9 +/- 0.08 microg/L), defined as very severe GHD; group 2 included 25 patients with a GH peak between 3.1-9 microg/L (4.7 +/- 0.4 microg/L), defined as severe GHD; group 3 included 18 patients with a GH peak between 9.1-16.5 microg/L (11.0 +/- 0.3 microg/L), defined as partial GHD; and group 4 included 17 patients with a GH peak above 16.5 microg/L (28.3 +/- 4.3 microg/L), defined as non-GHD. |
| 524 | 10372687 | In all 35 controls (group 5), the GH response after ARG+/-GHRH was above 16.5 microg/L (40.7 +/- 2.2 microg/L). |
| 525 | 10372687 | In patients in group 1, circulating IGF-I (P < 0.001), IGFBP-3 (P < 0.05), osteocalcin (P < 0.001), and urinary Ntx levels (P < 0.001) were lower than those in group 3-5, which were not different from each other; the t score at the lumbar spine (-1.99 +/- 0.2) and that at the femoral neck (-1.86 +/- 0.3) were lower than those in groups 3 (-0.5 +/- 0.7, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), 4 (-0.5 +/- 0.2, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), and 5 (-0.5 +/- 0.2, P < 0.001 and 0.0 +/- 0.02, P < 0.001, respectively). |
| 526 | 10372687 | In patients in group 2, circulating IGF-I and IGFBP-3 levels were not different from those in group 1, whereas the t scores at the lumbar spine (-1.22 +/- 0.3) and femoral neck (-0.9 +/- 0.3) were significantly higher and lower, respectively, than those in groups 1 and 5 (P < 0.05) but not those in groups 3 and 4, and serum osteocalcin and urinary Ntx levels were significant higher than those in group 1 and lower than those in groups 3-5 (P < 0.001). |
| 527 | 10372687 | MPHD, patients were subdivided according to the number of their hormonal deficits, such as panhypopituitarism with (10 patients) or without (31 patients) diabetes insipidus, GHD with 1 or more additional pituitary deficit(s) (36 patients), isolated GHD (7 patients), 1-2 pituitary hormone deficit(s) without GHD (10 patients), and normal anterior pituitary function (7 patients). |
| 528 | 10372687 | A significant correlation was found between the GH peak after ARG+GHRH and IGF-I, osteocalcin, urinary Ntx levels, and the t score at the lumbar spine, but not that at the femoral neck level. |
| 529 | 10372687 | A significant correlation was also found between plasma IGF-I levels and the t score at the lumbar spine and femoral neck, serum osteocalcin, and urinary Ntx. |
| 530 | 10372687 | Multiple correlation analysis revealed that the t score at the lumbar spine, but not that at the femoral neck, was more strongly predicted by plasma IGF-I levels (t = 3.376; P < 0.005) than by the GH peak after ARG+GHRH (t = -0.968; P = 0.338). |
| 531 | 10372687 | To investigate whether the severity of GHD was correlated with the degree of bone mass and turnover impairment, we evaluated BMD at the lumbar spine and femoral neck; circulating insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and osteocalcin levels, and urinary cross-linked N-telopeptides of type I collagen (Ntx) levels in 101 adult hypopituitary patients and 35 sex- and age-matched healthy subjects. |
| 532 | 10372687 | On the basis of the GH response to arginine plus GHRH (ARG+/-GHRH), patients were subdivided into 4 groups: group 1 included 41 patients with a GH peak below 3 microg/L (0.9 +/- 0.08 microg/L), defined as very severe GHD; group 2 included 25 patients with a GH peak between 3.1-9 microg/L (4.7 +/- 0.4 microg/L), defined as severe GHD; group 3 included 18 patients with a GH peak between 9.1-16.5 microg/L (11.0 +/- 0.3 microg/L), defined as partial GHD; and group 4 included 17 patients with a GH peak above 16.5 microg/L (28.3 +/- 4.3 microg/L), defined as non-GHD. |
| 533 | 10372687 | In all 35 controls (group 5), the GH response after ARG+/-GHRH was above 16.5 microg/L (40.7 +/- 2.2 microg/L). |
| 534 | 10372687 | In patients in group 1, circulating IGF-I (P < 0.001), IGFBP-3 (P < 0.05), osteocalcin (P < 0.001), and urinary Ntx levels (P < 0.001) were lower than those in group 3-5, which were not different from each other; the t score at the lumbar spine (-1.99 +/- 0.2) and that at the femoral neck (-1.86 +/- 0.3) were lower than those in groups 3 (-0.5 +/- 0.7, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), 4 (-0.5 +/- 0.2, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), and 5 (-0.5 +/- 0.2, P < 0.001 and 0.0 +/- 0.02, P < 0.001, respectively). |
| 535 | 10372687 | In patients in group 2, circulating IGF-I and IGFBP-3 levels were not different from those in group 1, whereas the t scores at the lumbar spine (-1.22 +/- 0.3) and femoral neck (-0.9 +/- 0.3) were significantly higher and lower, respectively, than those in groups 1 and 5 (P < 0.05) but not those in groups 3 and 4, and serum osteocalcin and urinary Ntx levels were significant higher than those in group 1 and lower than those in groups 3-5 (P < 0.001). |
| 536 | 10372687 | MPHD, patients were subdivided according to the number of their hormonal deficits, such as panhypopituitarism with (10 patients) or without (31 patients) diabetes insipidus, GHD with 1 or more additional pituitary deficit(s) (36 patients), isolated GHD (7 patients), 1-2 pituitary hormone deficit(s) without GHD (10 patients), and normal anterior pituitary function (7 patients). |
| 537 | 10372687 | A significant correlation was found between the GH peak after ARG+GHRH and IGF-I, osteocalcin, urinary Ntx levels, and the t score at the lumbar spine, but not that at the femoral neck level. |
| 538 | 10372687 | A significant correlation was also found between plasma IGF-I levels and the t score at the lumbar spine and femoral neck, serum osteocalcin, and urinary Ntx. |
| 539 | 10372687 | Multiple correlation analysis revealed that the t score at the lumbar spine, but not that at the femoral neck, was more strongly predicted by plasma IGF-I levels (t = 3.376; P < 0.005) than by the GH peak after ARG+GHRH (t = -0.968; P = 0.338). |
| 540 | 10372687 | To investigate whether the severity of GHD was correlated with the degree of bone mass and turnover impairment, we evaluated BMD at the lumbar spine and femoral neck; circulating insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and osteocalcin levels, and urinary cross-linked N-telopeptides of type I collagen (Ntx) levels in 101 adult hypopituitary patients and 35 sex- and age-matched healthy subjects. |
| 541 | 10372687 | On the basis of the GH response to arginine plus GHRH (ARG+/-GHRH), patients were subdivided into 4 groups: group 1 included 41 patients with a GH peak below 3 microg/L (0.9 +/- 0.08 microg/L), defined as very severe GHD; group 2 included 25 patients with a GH peak between 3.1-9 microg/L (4.7 +/- 0.4 microg/L), defined as severe GHD; group 3 included 18 patients with a GH peak between 9.1-16.5 microg/L (11.0 +/- 0.3 microg/L), defined as partial GHD; and group 4 included 17 patients with a GH peak above 16.5 microg/L (28.3 +/- 4.3 microg/L), defined as non-GHD. |
| 542 | 10372687 | In all 35 controls (group 5), the GH response after ARG+/-GHRH was above 16.5 microg/L (40.7 +/- 2.2 microg/L). |
| 543 | 10372687 | In patients in group 1, circulating IGF-I (P < 0.001), IGFBP-3 (P < 0.05), osteocalcin (P < 0.001), and urinary Ntx levels (P < 0.001) were lower than those in group 3-5, which were not different from each other; the t score at the lumbar spine (-1.99 +/- 0.2) and that at the femoral neck (-1.86 +/- 0.3) were lower than those in groups 3 (-0.5 +/- 0.7, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), 4 (-0.5 +/- 0.2, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), and 5 (-0.5 +/- 0.2, P < 0.001 and 0.0 +/- 0.02, P < 0.001, respectively). |
| 544 | 10372687 | In patients in group 2, circulating IGF-I and IGFBP-3 levels were not different from those in group 1, whereas the t scores at the lumbar spine (-1.22 +/- 0.3) and femoral neck (-0.9 +/- 0.3) were significantly higher and lower, respectively, than those in groups 1 and 5 (P < 0.05) but not those in groups 3 and 4, and serum osteocalcin and urinary Ntx levels were significant higher than those in group 1 and lower than those in groups 3-5 (P < 0.001). |
| 545 | 10372687 | MPHD, patients were subdivided according to the number of their hormonal deficits, such as panhypopituitarism with (10 patients) or without (31 patients) diabetes insipidus, GHD with 1 or more additional pituitary deficit(s) (36 patients), isolated GHD (7 patients), 1-2 pituitary hormone deficit(s) without GHD (10 patients), and normal anterior pituitary function (7 patients). |
| 546 | 10372687 | A significant correlation was found between the GH peak after ARG+GHRH and IGF-I, osteocalcin, urinary Ntx levels, and the t score at the lumbar spine, but not that at the femoral neck level. |
| 547 | 10372687 | A significant correlation was also found between plasma IGF-I levels and the t score at the lumbar spine and femoral neck, serum osteocalcin, and urinary Ntx. |
| 548 | 10372687 | Multiple correlation analysis revealed that the t score at the lumbar spine, but not that at the femoral neck, was more strongly predicted by plasma IGF-I levels (t = 3.376; P < 0.005) than by the GH peak after ARG+GHRH (t = -0.968; P = 0.338). |
| 549 | 10372687 | To investigate whether the severity of GHD was correlated with the degree of bone mass and turnover impairment, we evaluated BMD at the lumbar spine and femoral neck; circulating insulin-like growth factor I (IGF-I), IGF-binding protein-3 (IGFBP-3), and osteocalcin levels, and urinary cross-linked N-telopeptides of type I collagen (Ntx) levels in 101 adult hypopituitary patients and 35 sex- and age-matched healthy subjects. |
| 550 | 10372687 | On the basis of the GH response to arginine plus GHRH (ARG+/-GHRH), patients were subdivided into 4 groups: group 1 included 41 patients with a GH peak below 3 microg/L (0.9 +/- 0.08 microg/L), defined as very severe GHD; group 2 included 25 patients with a GH peak between 3.1-9 microg/L (4.7 +/- 0.4 microg/L), defined as severe GHD; group 3 included 18 patients with a GH peak between 9.1-16.5 microg/L (11.0 +/- 0.3 microg/L), defined as partial GHD; and group 4 included 17 patients with a GH peak above 16.5 microg/L (28.3 +/- 4.3 microg/L), defined as non-GHD. |
| 551 | 10372687 | In all 35 controls (group 5), the GH response after ARG+/-GHRH was above 16.5 microg/L (40.7 +/- 2.2 microg/L). |
| 552 | 10372687 | In patients in group 1, circulating IGF-I (P < 0.001), IGFBP-3 (P < 0.05), osteocalcin (P < 0.001), and urinary Ntx levels (P < 0.001) were lower than those in group 3-5, which were not different from each other; the t score at the lumbar spine (-1.99 +/- 0.2) and that at the femoral neck (-1.86 +/- 0.3) were lower than those in groups 3 (-0.5 +/- 0.7, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), 4 (-0.5 +/- 0.2, P < 0.01 and -0.3 +/- 0.7, P < 0.01, respectively), and 5 (-0.5 +/- 0.2, P < 0.001 and 0.0 +/- 0.02, P < 0.001, respectively). |
| 553 | 10372687 | In patients in group 2, circulating IGF-I and IGFBP-3 levels were not different from those in group 1, whereas the t scores at the lumbar spine (-1.22 +/- 0.3) and femoral neck (-0.9 +/- 0.3) were significantly higher and lower, respectively, than those in groups 1 and 5 (P < 0.05) but not those in groups 3 and 4, and serum osteocalcin and urinary Ntx levels were significant higher than those in group 1 and lower than those in groups 3-5 (P < 0.001). |
| 554 | 10372687 | MPHD, patients were subdivided according to the number of their hormonal deficits, such as panhypopituitarism with (10 patients) or without (31 patients) diabetes insipidus, GHD with 1 or more additional pituitary deficit(s) (36 patients), isolated GHD (7 patients), 1-2 pituitary hormone deficit(s) without GHD (10 patients), and normal anterior pituitary function (7 patients). |
| 555 | 10372687 | A significant correlation was found between the GH peak after ARG+GHRH and IGF-I, osteocalcin, urinary Ntx levels, and the t score at the lumbar spine, but not that at the femoral neck level. |
| 556 | 10372687 | A significant correlation was also found between plasma IGF-I levels and the t score at the lumbar spine and femoral neck, serum osteocalcin, and urinary Ntx. |
| 557 | 10372687 | Multiple correlation analysis revealed that the t score at the lumbar spine, but not that at the femoral neck, was more strongly predicted by plasma IGF-I levels (t = 3.376; P < 0.005) than by the GH peak after ARG+GHRH (t = -0.968; P = 0.338). |
| 558 | 10395678 | TCR and CD28 are coupled via ZAP-70 to the activation of the Vav/Rac-1-/PAK-1/p38 MAPK signaling pathway. |
| 559 | 10395678 | The small GTPase Rac-1 controls the catalytic activity of the mitogen-activated protein kinases (MAPKs) and cell cycle progression through G1. |
| 560 | 10395678 | Rac-1 activation requires the phospho-tyrosine (p-Tyr)-dependent recruitment of the Vav GDP releasing factor (GRF) to the plasma membrane and assembly of GTPase/GRF complexes, an event critical for Ag receptor-triggered T cell activation. |
| 561 | 10395678 | Here, we show that TCR/CD28 costimulation synergistically induces Rac-1 GDP/GTP exchange. |
| 562 | 10395678 | Our findings, obtained by using ZAP-70-negative Jurkat T cells, indicate that CD28 costimulation augments TCR-mediated T cell activation by increasing the ZAP-70-mediated Tyr phosphorylation of Vav. |
| 563 | 10395678 | This event regulates the Rac-1-associated GTP/GDP exchange activity of Vav and downstream pathway(s) leading to PAK-1 and p38 MAPK activation. |
| 564 | 10395678 | CD28 amplifies TCR-induced ZAP-70 activity and association of Vav with ZAP-70 and linker for activation of T cells (LAT). |
| 565 | 10395678 | These results favor a model in which ZAP-70 regulates the intersection of the TCR and CD28 signaling pathways, which elicits the coupling of TCR and CD28 to the Rac-1, PAK-1, and p38 MAPK effector molecules. |
| 566 | 10436815 | Pancreatic endocrine tumors (PET's) can be divided on a clinical and pathologic basis into ten classes [insulinomas, gastrinomas (Zollinger-Ellison syndrome), VIPomas (Verner-Morrison syndrome, WDHA, pancreatic cholera), glucagonomas, somatostatinomas, ACTH-releasing tumors (ACTHomas), growth hormone-releasing factor secreting tumors (GRFomas), nonfunctioning or pancreatic polypeptide secreting tumors (non-functioning PET), PET's causing carcinoid syndrome and PET's causing hypercalcemia)]. |
| 567 | 10644563 | Rat and guinea pig pancreatic acini possess both VIP(1) and VIP(2) receptors, which mediate enzyme secretion. |
| 568 | 10644563 | At low concentrations (10 nM) of Ro-25-1553 and [Lys(15),Arg(16), Leu(27)]VIP-(1-7)-GRF(8-27), which only occupy VIP receptors, a 4-fold and a 56-fold increase in cAMP occurred, respectively. |
| 569 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 570 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 571 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 572 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 573 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 574 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 575 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 576 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 577 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 578 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 579 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 580 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 581 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 582 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 583 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 584 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 585 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 586 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 587 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 588 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 589 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 590 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 591 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 592 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 593 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 594 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 595 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 596 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 597 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 598 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 599 | 10692141 | Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. |
| 600 | 10692141 | However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. |
| 601 | 10692141 | We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. |
| 602 | 10692141 | Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). |
| 603 | 10692141 | A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. |
| 604 | 10692141 | These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression. |
| 605 | 10720081 | In the present study, 10 patients (3 men and 7 women, aged 48-63 yr) with an adrenal mass discovered serendipitously underwent, on separate occasions, a GHRH injection alone or combined with an infusion of the functional somatostatin antagonist, arginine. |
| 606 | 10720081 | In summary, the present data suggest that in patients with incidental adrenal adenomas the GH response to GHRH is blunted due to increased somatostatinergic tone, as it can be restored to normal by pretreatment with the functional somatostatin antagonist arginine. |
| 607 | 10720081 | In the present study, 10 patients (3 men and 7 women, aged 48-63 yr) with an adrenal mass discovered serendipitously underwent, on separate occasions, a GHRH injection alone or combined with an infusion of the functional somatostatin antagonist, arginine. |
| 608 | 10720081 | In summary, the present data suggest that in patients with incidental adrenal adenomas the GH response to GHRH is blunted due to increased somatostatinergic tone, as it can be restored to normal by pretreatment with the functional somatostatin antagonist arginine. |
| 609 | 10830243 | Serum insulin levels were significantly higher in IDDUP compared to UVEST (P=0.05) both at baseline and post GH-RH stimulus, while were similar to KPTx (P=0.2) and UVESTCY (P=0.7). |
| 610 | 10830243 | Our results indicate that: 1) kidney-pancreas transplantation does not normalize the GH response to GH-RH; 2) GH abnormalities are not due either to the chronic immunosuppressive therapy or to the insulin effect on GH release; 3) GH abnormalities are probably secondary to functional and/or organic complications of the hypothalamus and/or pituitary as a sequela of diabetes mellitus. |
| 611 | 10830243 | Serum insulin levels were significantly higher in IDDUP compared to UVEST (P=0.05) both at baseline and post GH-RH stimulus, while were similar to KPTx (P=0.2) and UVESTCY (P=0.7). |
| 612 | 10830243 | Our results indicate that: 1) kidney-pancreas transplantation does not normalize the GH response to GH-RH; 2) GH abnormalities are not due either to the chronic immunosuppressive therapy or to the insulin effect on GH release; 3) GH abnormalities are probably secondary to functional and/or organic complications of the hypothalamus and/or pituitary as a sequela of diabetes mellitus. |
| 613 | 10841459 | The post-prandial increase of glucose concentrations was significantly smaller, of lactate tended to be smaller, and growth hormone peak frequency tended to be lower, whereas maximal insulin concentrations reached post-prandially were significantly higher in GrF than GrC. |
| 614 | 11291426 | Contribution of growth hormone-releasing hormone and somatostatin to decreased growth hormone secretion in elderly men. |
| 615 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 616 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 617 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 618 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 619 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 620 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 621 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 622 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 623 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 624 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 625 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 626 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 627 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 628 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 629 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 630 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 631 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 632 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 633 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 634 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 635 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 636 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 637 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 638 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 639 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 640 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 641 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 642 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 643 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 644 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 645 | 11445245 | GI side-effects of a possible therapeutic GRF analogue in monkeys are likely due to VIP receptor agonist activity. |
| 646 | 11445245 | Because GRF has similarity to VIP/PACAP and VIPomas cause diarrhea, this study investigated the ability of this and other GRF analogues to interact with the VIP/PACAP receptors. |
| 647 | 11445245 | Rat VPAC(1)-R (rVPAC(1)-R), human VPAC(1)-R (hVPAC(1)-R), rVPAC(2)-R and hVPAC(2)-R stably transfected CHO and PANC 1 cells were made and T47D breast cancer cells containing native human VPAC(1)-R and AR4-2J cells containing PAC(1)-R were used. hGRF(1-29)NH(2) had low affinity for both rVPAC(1)-R and rVPAC(2)-R while VIP had a high affinity for both receptors. |
| 648 | 11445245 | VIP had a high affinity, whereas hGRF(1-29)NH(2) had a low affinity for both hVPAC(1)-R and hVPAC(2)-R. |
| 649 | 11445245 | These results demonstrate that in contrast to native hGRF(1-29)NH(2,) GRF-6 has a relatively high affinity for the human VPAC(1)-R but not for the human VPAC(2)-R, rat VPAC(1)-R, rat VPAC(2)-R or rat PAC(1)-R. |
| 650 | 11445245 | Furthermore, they demonstrate significant species differences can exist for possible therapeutic peptide agonists of the VIP/PACAP/GRF receptor family and that it is essential that receptor affinity assessments be performed in human cells or from a closely related species. |
| 651 | 11994347 | Two stimulatory tests for GH secretion were employed: insulin tolerance test (ITT, 0.15 IU/kg regular insulin i.v. bolus); and GHRH+GHRP-6 test: GHRH (Geref Serono, Madrid, Spain; l microg/kg) plus GHRP-6 (CLINALFA, Laufelingen, Switzerland; 1 microg/kg) as i.v. bolus. |
| 652 | 12058343 | The diagnosis was confirmed by elevated GH, IGF-1 and GHRH secretion. |
| 653 | 12397533 | Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. |
| 654 | 12397533 | GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. |
| 655 | 12397533 | Cells were incubated for 3 or 5 days with or without phytohemagglutinin (PHA-M), GHRH, GHRP-6 analogue hexarelin, somatostatin or GHRH + hexarelin. |
| 656 | 12397533 | GHRH stimulated lymphocytic GH secretion, whereas, somatostatin had no effect. |
| 657 | 12841541 | The objective of our study was to assess the effect of short-term fasting on GH response to combined stimulus with GHRH+GH-releasing peptide-6 (GHRP-6) in obese patients with PCOS and possible relation with leptin and insulin changes during fasting. |
| 658 | 12841541 | GH response, IGF-I, insulin and leptin were measured after GHRH+ GHRP-6, before and after short-term fasting. |
| 659 | 12841541 | Insulin and leptin significantly decreased, while insulin sensitivity significantly improved in both groups during fasting. |
| 660 | 12841541 | Observed changes in insulin and leptin may participate in modulation of enhanced GH response after short-term fasting to GHRH+GHRP-6 in PCOS and obese controls. |
| 661 | 12841541 | The objective of our study was to assess the effect of short-term fasting on GH response to combined stimulus with GHRH+GH-releasing peptide-6 (GHRP-6) in obese patients with PCOS and possible relation with leptin and insulin changes during fasting. |
| 662 | 12841541 | GH response, IGF-I, insulin and leptin were measured after GHRH+ GHRP-6, before and after short-term fasting. |
| 663 | 12841541 | Insulin and leptin significantly decreased, while insulin sensitivity significantly improved in both groups during fasting. |
| 664 | 12841541 | Observed changes in insulin and leptin may participate in modulation of enhanced GH response after short-term fasting to GHRH+GHRP-6 in PCOS and obese controls. |
| 665 | 12841541 | The objective of our study was to assess the effect of short-term fasting on GH response to combined stimulus with GHRH+GH-releasing peptide-6 (GHRP-6) in obese patients with PCOS and possible relation with leptin and insulin changes during fasting. |
| 666 | 12841541 | GH response, IGF-I, insulin and leptin were measured after GHRH+ GHRP-6, before and after short-term fasting. |
| 667 | 12841541 | Insulin and leptin significantly decreased, while insulin sensitivity significantly improved in both groups during fasting. |
| 668 | 12841541 | Observed changes in insulin and leptin may participate in modulation of enhanced GH response after short-term fasting to GHRH+GHRP-6 in PCOS and obese controls. |
| 669 | 14693411 | GH response to i.v. bolus of GHRH+GHRP-6 (100 mcg, each) was measured in 12 male patients with type 2 diabetes (mean age: 53.9+/-1.59 years; BMI: 25.58+/-0.39 kg/m(2); mean HbA(1c): 8.7+/-0.42%), during a euglycemic (mean glucose: 4.92+/-0.08 mmol) hyperinsulinemic clamp (insulin infusion rate of 100 mU/kg/h) and a hyperglycemic clamp (mean glucose: 12.19+/-0.11 mmol/l). |
| 670 | 14715864 | In vitro data have recently suggested that sulfonylureas (SUs) enhance GH secretion by modulating the effects of GHRH and somatostatin in pituitary cells. |
| 671 | 14715864 | Subsequently, GH concentrations were measured regularly after stimulation with GHRH (bolus 0.1 micro g/kg) alone and during concomitant infusion with somatostatin (7 ng.kg(-1).min(-1)). |
| 672 | 14715864 | In vitro data have recently suggested that sulfonylureas (SUs) enhance GH secretion by modulating the effects of GHRH and somatostatin in pituitary cells. |
| 673 | 14715864 | Subsequently, GH concentrations were measured regularly after stimulation with GHRH (bolus 0.1 micro g/kg) alone and during concomitant infusion with somatostatin (7 ng.kg(-1).min(-1)). |
| 674 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 675 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 676 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 677 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 678 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 679 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 680 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 681 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 682 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 683 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 684 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 685 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 686 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 687 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 688 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 689 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 690 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 691 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 692 | 14997011 | Modulation of brain insulin-like growth factor I (IGF-I) binding sites and hypothalamic GHRH and somatostatin levels by exogenous growth hormone and IGF-I in juvenile rats. |
| 693 | 14997011 | The effect of exogenous growth hormone (GH) and insulin-like growth factor I (IGF-I) on brain IGF-I binding sites (IGF-IR), and on the levels of growth hormone-releasing hormone (GHRH) and somatostatin was studied in hypophysectomized and intact juvenile male rats. |
| 694 | 14997011 | There was a significant increase in IGF-IR binding capacity in the IGF-I-treated hypophysectomized rats compared to the saline-treated hypophysectomized animals (150.61 +/- 45.66 vs 41.32 +/- 12.42 fmol/mg, p < 0.05) but no significant difference in IGF-IR mRNA levels. |
| 695 | 14997011 | GHRH levels in the saline-treated hypophysectomized group were significantly lower than in the saline-treated intact rats (31.2 +/- 11.2 vs 140.6 +/- 48.1 pg/mg tissue, respectively, p < 0.01); no effect was induced by GH or IGF-I (37.5 +/- 26.8 and 53.8 +/- 22.5 pg/mg tissue, respectively). |
| 696 | 14997011 | However, in the intact rats, GH and IGF-I injection led to a decrease in GHRH content, which was significant in the GH-treated compared to the saline-treated animals (33.1 +/- 16.2 vs 140.6 +/- 48.1 pg/mg tissue, p < 0.01). |
| 697 | 14997011 | However, in the hypophysectomized animals, GH and IGF-I treatment induced a significant increase in somatostatin levels (1300 +/- 193.7 pg/mg tissue, p < 0.01, and 912.5 +/- 81.2 pg/mg tissue, p < 0.05, respectively). |
| 698 | 15456744 | Recent studies using knock-out mice have shown that animals can develop relatively normally with deficiency for each of the G1/S-regulatory proteins, D-type and E-type cyclins, cyclin-dependent kinase 4 (Cdk4), and Cdk2. |
| 699 | 15456744 | Pituitary hyperplasia induced by transgenic expression of human growth hormone-releasing hormone (GHRH) is significantly diminished in the Cdk4+/- genetic background and completely abrogated in the Cdk4-/- background. |
| 700 | 15456744 | Small interfering RNA (siRNA)-mediated knockdown of Cdk4 inhibits GHRH-induced proliferation of GH3 somato/lactotroph cells with restored expression of GHRH receptors. |
| 701 | 15456744 | Furthermore, Cdk4 siRNA does not affect GHRH-induced proliferation of mouse embryonic fibroblasts or estrogen-dependent proliferation of mammary carcinoma MCF-7 cells. |
| 702 | 15456744 | Recent studies using knock-out mice have shown that animals can develop relatively normally with deficiency for each of the G1/S-regulatory proteins, D-type and E-type cyclins, cyclin-dependent kinase 4 (Cdk4), and Cdk2. |
| 703 | 15456744 | Pituitary hyperplasia induced by transgenic expression of human growth hormone-releasing hormone (GHRH) is significantly diminished in the Cdk4+/- genetic background and completely abrogated in the Cdk4-/- background. |
| 704 | 15456744 | Small interfering RNA (siRNA)-mediated knockdown of Cdk4 inhibits GHRH-induced proliferation of GH3 somato/lactotroph cells with restored expression of GHRH receptors. |
| 705 | 15456744 | Furthermore, Cdk4 siRNA does not affect GHRH-induced proliferation of mouse embryonic fibroblasts or estrogen-dependent proliferation of mammary carcinoma MCF-7 cells. |
| 706 | 15456744 | Recent studies using knock-out mice have shown that animals can develop relatively normally with deficiency for each of the G1/S-regulatory proteins, D-type and E-type cyclins, cyclin-dependent kinase 4 (Cdk4), and Cdk2. |
| 707 | 15456744 | Pituitary hyperplasia induced by transgenic expression of human growth hormone-releasing hormone (GHRH) is significantly diminished in the Cdk4+/- genetic background and completely abrogated in the Cdk4-/- background. |
| 708 | 15456744 | Small interfering RNA (siRNA)-mediated knockdown of Cdk4 inhibits GHRH-induced proliferation of GH3 somato/lactotroph cells with restored expression of GHRH receptors. |
| 709 | 15456744 | Furthermore, Cdk4 siRNA does not affect GHRH-induced proliferation of mouse embryonic fibroblasts or estrogen-dependent proliferation of mammary carcinoma MCF-7 cells. |
| 710 | 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. |
| 711 | 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. |
| 712 | 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. |
| 713 | 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. |
| 714 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 715 | 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. |
| 716 | 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. |
| 717 | 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. |
| 718 | 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. |
| 719 | 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. |
| 720 | 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. |
| 721 | 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. |
| 722 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 723 | 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. |
| 724 | 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. |
| 725 | 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. |
| 726 | 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. |
| 727 | 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. |
| 728 | 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. |
| 729 | 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. |
| 730 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 731 | 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. |
| 732 | 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. |
| 733 | 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. |
| 734 | 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. |
| 735 | 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. |
| 736 | 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. |
| 737 | 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. |
| 738 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 739 | 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. |
| 740 | 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. |
| 741 | 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. |
| 742 | 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. |
| 743 | 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. |
| 744 | 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. |
| 745 | 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. |
| 746 | 15662591 | Stimulation of LHbeta mRNA by GnRH was suppressed by inactivation of AC or of PKC but not by inactivation of PKA. |
| 747 | 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. |
| 748 | 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. |
| 749 | 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. |
| 750 | 16075928 | Circulating insulin-like growth factor-I levels are correlated with the atherosclerotic profile in healthy subjects independently of age. |
| 751 | 16075928 | Peak GH after GHRH+arginine (ARG) test, serum IGF-I and IGF binding protein-3 (IGFBP-3), lipid profile, homeostasis model assessment (HOMA) index and intima-media thickness (IMT) at common carotid arteries were measured in 174 healthy individuals (92 women, 82 men, aged 18-80 yr). |
| 752 | 16075928 | An inverse correlation was found between the IGF-I z-score and total/HDL-cholesterol ratio (p = 0.02) and mean IMT (p = 0.0009); IGFBP-3 z-score and mean IMT (p = 0.043); IGF: IGFBP-3 molar ratio and total/HDL-cholesterol ratio (p < 0.0001) and mean IMT (p < 0.0001). |
| 753 | 16075928 | At multi-step regression analysis, age was the best predictor of HDL-cholesterol levels and mean IMT, IGF-I level was the best predictor of total cholesterol and total/HDL-cholesterol ratio, the IGF-I/IGFBP-3 molar ratio was the best predictor of triglycerides levels. |
| 754 | 16075928 | The z-scores of IGF-I and IGFBP-3 were the second best predictors of mean IMT after age. |
| 755 | 16075928 | In conclusion, IGF-I and IGFBP-3 were negatively correlated with common cardiovascular risk factors, studied as total/HDL-cholesterol ratio, and/or early atherosclerosis, studied as IMT at common carotid arteries. |
| 756 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 757 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 758 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 759 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 760 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 761 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 762 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 763 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 764 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 765 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 766 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 767 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 768 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 769 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 770 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 771 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 772 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 773 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 774 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 775 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 776 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 777 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 778 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 779 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 780 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 781 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 782 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 783 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 784 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 785 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 786 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 787 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 788 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 789 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 790 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 791 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 792 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 793 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 794 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 795 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 796 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 797 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 798 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 799 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 800 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 801 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 802 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 803 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 804 | 16244497 | These changes are believed to be due to a rise in hypothalamic neuropeptide Y (NPY) that inhibits GHRH expression. |
| 805 | 16244497 | To directly test if NPY is required for metabolic regulation of hypothalamic neuropeptides important in GH secretion, NPY, GHRH and somatostatin (SRIH) mRNA levels were determined in fasted (48 h) and STZ-treated wild-type (NPY(+/+)) and NPY-knockout (NPY(-/-)) mice by ribonuclease protection assay. |
| 806 | 16244497 | In addition, pituitary receptor mRNA levels for GHRH (GHRH-R), ghrelin (GHS-R) and SRIH (sst2) were assessed by RT-PCR. |
| 807 | 16244497 | In the NPY(+/+) mouse, fasting resulted in a 23% weight loss and >250% increase in NPY mRNA accompanied by a significant reduction in both GHRH and SRIH mRNA. |
| 808 | 16244497 | These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2. |
| 809 | 16244497 | In the NPY(-/-) mouse, fasting also resulted in a 23% weight loss and comparable changes in GHRH-R and sst2, but failed to alter GHRH, SRIH and GHS-R mRNA levels. |
| 810 | 16244497 | Induction of diabetes in NPY(+/+) mice, using a single, high-dose, STZ injection (150 mg/kg), resulted in modest weight loss (5%), and a 158% increase NPY expression which was associated with reciprocal changes in pituitary GHS-R and sst2 expression, similar to that observed in the fasted state, but no change in hypothalamic GHRH or SRIF expression was observed. |
| 811 | 16244497 | These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA. |
| 812 | 16461552 | As previously reported, HI STZ resulted in a decrease in circulating GH and IGF-I levels which was associated with a rise in hypothalamic neuropeptide Y (NPY) mRNA (355% of vehicle-treated controls) and a fall in GH-releasing hormone (GHRH) mRNA (45% of vehicle-treated controls) levels. |
| 813 | 16461552 | Changes in hypothalamic neuropeptide expression were reflected by an increase in immunoreactive NPY within the arcuate and paraventricular nuclei and a decrease in GHRH immunoreactivity in the arcuate nucleus, as assessed by immunohistochemistry. |
| 814 | 16461552 | However, pituitary receptor mRNA levels for GHRH and ghrelin increased and those for somatostatin (sst2, sst3 and sst5) decreased following HI STZ treatment. |
| 815 | 16461552 | Specifically, LO STZ treatment did suppress circulating IGF-I levels to the same extent as HI STZ treatment; however, the impact on hypothalamic NPY mRNA levels was less dramatic (158% of vehicle-treated controls) where NPY immunoreactivity was increased only within the paraventricular nucleus. |
| 816 | 16461552 | As previously reported, HI STZ resulted in a decrease in circulating GH and IGF-I levels which was associated with a rise in hypothalamic neuropeptide Y (NPY) mRNA (355% of vehicle-treated controls) and a fall in GH-releasing hormone (GHRH) mRNA (45% of vehicle-treated controls) levels. |
| 817 | 16461552 | Changes in hypothalamic neuropeptide expression were reflected by an increase in immunoreactive NPY within the arcuate and paraventricular nuclei and a decrease in GHRH immunoreactivity in the arcuate nucleus, as assessed by immunohistochemistry. |
| 818 | 16461552 | However, pituitary receptor mRNA levels for GHRH and ghrelin increased and those for somatostatin (sst2, sst3 and sst5) decreased following HI STZ treatment. |
| 819 | 16461552 | Specifically, LO STZ treatment did suppress circulating IGF-I levels to the same extent as HI STZ treatment; however, the impact on hypothalamic NPY mRNA levels was less dramatic (158% of vehicle-treated controls) where NPY immunoreactivity was increased only within the paraventricular nucleus. |
| 820 | 16461552 | As previously reported, HI STZ resulted in a decrease in circulating GH and IGF-I levels which was associated with a rise in hypothalamic neuropeptide Y (NPY) mRNA (355% of vehicle-treated controls) and a fall in GH-releasing hormone (GHRH) mRNA (45% of vehicle-treated controls) levels. |
| 821 | 16461552 | Changes in hypothalamic neuropeptide expression were reflected by an increase in immunoreactive NPY within the arcuate and paraventricular nuclei and a decrease in GHRH immunoreactivity in the arcuate nucleus, as assessed by immunohistochemistry. |
| 822 | 16461552 | However, pituitary receptor mRNA levels for GHRH and ghrelin increased and those for somatostatin (sst2, sst3 and sst5) decreased following HI STZ treatment. |
| 823 | 16461552 | Specifically, LO STZ treatment did suppress circulating IGF-I levels to the same extent as HI STZ treatment; however, the impact on hypothalamic NPY mRNA levels was less dramatic (158% of vehicle-treated controls) where NPY immunoreactivity was increased only within the paraventricular nucleus. |
| 824 | 16611045 | One of the most likely future applications, however, may be in intramuscular gene transfer for systemic delivery of either endocrine hormones (e.g., growth hormone releasing hormone and leptin), hematopoietic factors (e.g., erythropoietin, GM-CSF), antibodies, enzymes, or numerous other protein drugs. |
| 825 | 16644867 | However, Pc1 knockout mice do not become obese; in fact, they are runted due to a defect in growth-hormone releasing hormone processing, leading to the speculation that PC1 subserves different functions between mouse and human. |
| 826 | 16644867 | Here, we report a novel allele of mouse Pc1 (N222D) that leads to obesity, abnormal proinsulin processing and multiple endocrinological defects. |
| 827 | 16644867 | The obesity is associated with impaired autocatalytic activation of mature PC1 and reduced hypothalamic alpha-MSH. |
| 828 | 16868891 | To address this issue, we determine the prevalence of neuroendocrine abnormalities in patients rehabilitating from severe traumatic brain injury (Glasgow Coma Scale < or = 8). 76 patients (mean age 39 +/- 14 yr; range 18-65; 53 males and 23 females; BMI 25.8 +/- 4.2 kg/m2; mean +/- SD) with a severe traumatic brain injury, an average of 22 +/- 10 months before this study (median, 20 months), underwent a series of standard endocrine tests, including TSH, free T4, T4, T3, prolactin, testosterone (males), estradiol (females), cortisol, ACTH, GH, and IGF-I. |
| 829 | 16868891 | Pituitary deficiency was shown in 24% of the patients (18/76). 8% (n = 6) had GHD (GH-peak range [GHRH + arginine]: 2.8-6.3 microg/L; GH-peak range [ITT]: 1.5-2.2 microg/L; IGF-I range: 62-174 microg/L). 17% (n = 13) had hypogonadism (total testosterone < 9.5 nmol/L and low gonadotropins in 12 males; low estradiol, and low gonadotropins in 1 female). |
| 830 | 16946406 | The enzyme dipeptidyl peptidase-IV (DPP-IV) inactivates a variety of bioactive peptides, including glucagon-like peptide-1 (GLP-1) and growth hormone releasing hormone (GHRH). |
| 831 | 16946406 | Inhibiting DPP-IV in order to increase circulating GLP-1 is of interest as a treatment for Type II diabetes. |
| 832 | 16946406 | Inactivation of DPP-IV may also increase circulating GHRH, potentially enhancing growth in domestic animals. |
| 833 | 16946406 | To test the hypothesis that inhibition of DPP-IV activity will influence the growth hormone/ IGF-1 axis, growing pigs (Sus scrofa domesticus, 78 kg) were treated with a DPP-IV inhibitor (Compound 1, the 2,5-difluor-ophenyl analog of the triazolopiperazine MK0431, sitagliptin), and plasma concentrations of IGF-1 were monitored. |
| 834 | 16946406 | GHRH treatment increased the IGF-1 AUC (1210 +/- 160 ng/ml x hr, P = 0.049 vs. controls and P = 0.001 vs. |
| 835 | 16946406 | We conclude that inhibition of DPP-IV does not alter the circulating levels of IGF-1 in the growing pig. |
| 836 | 16946406 | The enzyme dipeptidyl peptidase-IV (DPP-IV) inactivates a variety of bioactive peptides, including glucagon-like peptide-1 (GLP-1) and growth hormone releasing hormone (GHRH). |
| 837 | 16946406 | Inhibiting DPP-IV in order to increase circulating GLP-1 is of interest as a treatment for Type II diabetes. |
| 838 | 16946406 | Inactivation of DPP-IV may also increase circulating GHRH, potentially enhancing growth in domestic animals. |
| 839 | 16946406 | To test the hypothesis that inhibition of DPP-IV activity will influence the growth hormone/ IGF-1 axis, growing pigs (Sus scrofa domesticus, 78 kg) were treated with a DPP-IV inhibitor (Compound 1, the 2,5-difluor-ophenyl analog of the triazolopiperazine MK0431, sitagliptin), and plasma concentrations of IGF-1 were monitored. |
| 840 | 16946406 | GHRH treatment increased the IGF-1 AUC (1210 +/- 160 ng/ml x hr, P = 0.049 vs. controls and P = 0.001 vs. |
| 841 | 16946406 | We conclude that inhibition of DPP-IV does not alter the circulating levels of IGF-1 in the growing pig. |
| 842 | 16946406 | The enzyme dipeptidyl peptidase-IV (DPP-IV) inactivates a variety of bioactive peptides, including glucagon-like peptide-1 (GLP-1) and growth hormone releasing hormone (GHRH). |
| 843 | 16946406 | Inhibiting DPP-IV in order to increase circulating GLP-1 is of interest as a treatment for Type II diabetes. |
| 844 | 16946406 | Inactivation of DPP-IV may also increase circulating GHRH, potentially enhancing growth in domestic animals. |
| 845 | 16946406 | To test the hypothesis that inhibition of DPP-IV activity will influence the growth hormone/ IGF-1 axis, growing pigs (Sus scrofa domesticus, 78 kg) were treated with a DPP-IV inhibitor (Compound 1, the 2,5-difluor-ophenyl analog of the triazolopiperazine MK0431, sitagliptin), and plasma concentrations of IGF-1 were monitored. |
| 846 | 16946406 | GHRH treatment increased the IGF-1 AUC (1210 +/- 160 ng/ml x hr, P = 0.049 vs. controls and P = 0.001 vs. |
| 847 | 16946406 | We conclude that inhibition of DPP-IV does not alter the circulating levels of IGF-1 in the growing pig. |
| 848 | 17072234 | Responses to ACTH or GHRH-arginine tests may be normal for several years though an ACTH and/or GH deficiency has been demonstrated by an insulin tolerance test, which is considered as the gold standard. |
| 849 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 850 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 851 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 852 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 853 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 854 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 855 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 856 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 857 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 858 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 859 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 860 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 861 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 862 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 863 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 864 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 865 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 866 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 867 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 868 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 869 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 870 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 871 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 872 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 873 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 874 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 875 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 876 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 877 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 878 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 879 | 17540720 | Evidence that ghrelin is as potent as growth hormone (GH)-releasing hormone (GHRH) in releasing GH from primary pituitary cell cultures of a nonhuman primate (Papio anubis), acting through intracellular signaling pathways distinct from GHRH. |
| 880 | 17540720 | Ghrelin is more effective than GHRH in stimulating GH release in normal adult humans and monkeys in vivo. |
| 881 | 17540720 | This robust effect of ghrelin has been largely attributed to regulation of hypothalamic input, whereas the direct effect of ghrelin on pituitary GH release has been minimized by the observation that ghrelin has only a modest impact on GH release, compared with GHRH, in cultures prepared from human fetal pituitaries and GH-producing adenomas, as well as pituitaries from nonprimate species. |
| 882 | 17540720 | In this model, both ghrelin and GHRH increased GH release in a dose-dependent fashion. |
| 883 | 17540720 | Surprisingly, at maximal concentrations (10 nM), both ghrelin and GHRH elicited a robust increase in GH release (4 and 24 h, respectively), and both up-regulated GH secretagogue-receptor and GHRH-receptor mRNA levels (24 h). |
| 884 | 17540720 | Combined treatment with ghrelin and GHRH resulted in an additive effect on GH release, suggesting that distinct intracellular signaling pathways are activated by each ligand, as confirmed by the use of specific inhibitors of intracellular signaling. |
| 885 | 17556866 | Ghrelin improves growth hormone responses to growth hormone-releasing hormone in a streptozotocin-diabetic model of delayed onset. |
| 886 | 17556866 | In the present study, we wanted to address the GH responses to GHRH and low doses of ghrelin in a streptozotocin (STZ) model of diabetes characterized by the delayed onset of the metabolic alterations. |
| 887 | 17556866 | At the age of 3 months, in these n5-STZ male and female rats the GH responses to GHRH (1 microg/kg) and GHRH combined with ghrelin (1+3 microg/kg) had diminished both in punctual times and in the area under the curve (AUC). |
| 888 | 17556866 | However, the combined administration of GHRH and ghrelin, being the more potent stimulus, elicited a synergistic GH response. |
| 889 | 17556866 | Thus, male and female rats with delayed onset diabetes displayed an altered GH response to GHRH, although the combined administration of GHRH and ghrelin was able to restore the GH secretion with a synergistic effect. |
| 890 | 17556866 | Ghrelin improves growth hormone responses to growth hormone-releasing hormone in a streptozotocin-diabetic model of delayed onset. |
| 891 | 17556866 | In the present study, we wanted to address the GH responses to GHRH and low doses of ghrelin in a streptozotocin (STZ) model of diabetes characterized by the delayed onset of the metabolic alterations. |
| 892 | 17556866 | At the age of 3 months, in these n5-STZ male and female rats the GH responses to GHRH (1 microg/kg) and GHRH combined with ghrelin (1+3 microg/kg) had diminished both in punctual times and in the area under the curve (AUC). |
| 893 | 17556866 | However, the combined administration of GHRH and ghrelin, being the more potent stimulus, elicited a synergistic GH response. |
| 894 | 17556866 | Thus, male and female rats with delayed onset diabetes displayed an altered GH response to GHRH, although the combined administration of GHRH and ghrelin was able to restore the GH secretion with a synergistic effect. |
| 895 | 17556866 | Ghrelin improves growth hormone responses to growth hormone-releasing hormone in a streptozotocin-diabetic model of delayed onset. |
| 896 | 17556866 | In the present study, we wanted to address the GH responses to GHRH and low doses of ghrelin in a streptozotocin (STZ) model of diabetes characterized by the delayed onset of the metabolic alterations. |
| 897 | 17556866 | At the age of 3 months, in these n5-STZ male and female rats the GH responses to GHRH (1 microg/kg) and GHRH combined with ghrelin (1+3 microg/kg) had diminished both in punctual times and in the area under the curve (AUC). |
| 898 | 17556866 | However, the combined administration of GHRH and ghrelin, being the more potent stimulus, elicited a synergistic GH response. |
| 899 | 17556866 | Thus, male and female rats with delayed onset diabetes displayed an altered GH response to GHRH, although the combined administration of GHRH and ghrelin was able to restore the GH secretion with a synergistic effect. |
| 900 | 17556866 | Ghrelin improves growth hormone responses to growth hormone-releasing hormone in a streptozotocin-diabetic model of delayed onset. |
| 901 | 17556866 | In the present study, we wanted to address the GH responses to GHRH and low doses of ghrelin in a streptozotocin (STZ) model of diabetes characterized by the delayed onset of the metabolic alterations. |
| 902 | 17556866 | At the age of 3 months, in these n5-STZ male and female rats the GH responses to GHRH (1 microg/kg) and GHRH combined with ghrelin (1+3 microg/kg) had diminished both in punctual times and in the area under the curve (AUC). |
| 903 | 17556866 | However, the combined administration of GHRH and ghrelin, being the more potent stimulus, elicited a synergistic GH response. |
| 904 | 17556866 | Thus, male and female rats with delayed onset diabetes displayed an altered GH response to GHRH, although the combined administration of GHRH and ghrelin was able to restore the GH secretion with a synergistic effect. |
| 905 | 17556866 | Ghrelin improves growth hormone responses to growth hormone-releasing hormone in a streptozotocin-diabetic model of delayed onset. |
| 906 | 17556866 | In the present study, we wanted to address the GH responses to GHRH and low doses of ghrelin in a streptozotocin (STZ) model of diabetes characterized by the delayed onset of the metabolic alterations. |
| 907 | 17556866 | At the age of 3 months, in these n5-STZ male and female rats the GH responses to GHRH (1 microg/kg) and GHRH combined with ghrelin (1+3 microg/kg) had diminished both in punctual times and in the area under the curve (AUC). |
| 908 | 17556866 | However, the combined administration of GHRH and ghrelin, being the more potent stimulus, elicited a synergistic GH response. |
| 909 | 17556866 | Thus, male and female rats with delayed onset diabetes displayed an altered GH response to GHRH, although the combined administration of GHRH and ghrelin was able to restore the GH secretion with a synergistic effect. |
| 910 | 17898534 | Ghrelin is best known for its hypothalamic actions on growth hormone-releasing hormone neurons and neuropeptide Y/agouti-related peptide neurons; however, ghrelin affects multiple organ systems and the complexity of its functions is only now being realized. |
| 911 | 17898534 | A reciprocal relationship exists between ghrelin and insulin, suggesting that ghrelin regulates glucose homeostasis. |
| 912 | 17898534 | Ablation of ghrelin in mice increases glucose-induced insulin secretion, and improves peripheral insulin sensitivity. |
| 913 | 18095239 | To test whether a similar mechanism could explain the enhanced Growth Hormone (GH) secretory response to GH-Releasing Hormone (GHRH), which is seen in human LC, we studied the effect of the cholinesterase inhibitor pyridostigmine (PD), which is able to reduce the release of hypothalamic somatostatin (SS), on the GHRH-stimulated GH secretion. |
| 914 | 18285528 | Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity. |
| 915 | 18285528 | The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. |
| 916 | 18285528 | Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. |
| 917 | 18285528 | Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16-24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. |
| 918 | 18285528 | Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. |
| 919 | 18285528 | Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. |
| 920 | 18285528 | Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity. |
| 921 | 18285528 | The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. |
| 922 | 18285528 | Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. |
| 923 | 18285528 | Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16-24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. |
| 924 | 18285528 | Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. |
| 925 | 18285528 | Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. |
| 926 | 18285528 | Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity. |
| 927 | 18285528 | The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. |
| 928 | 18285528 | Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. |
| 929 | 18285528 | Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16-24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. |
| 930 | 18285528 | Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. |
| 931 | 18285528 | Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. |
| 932 | 18285528 | Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity. |
| 933 | 18285528 | The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. |
| 934 | 18285528 | Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. |
| 935 | 18285528 | Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16-24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. |
| 936 | 18285528 | Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. |
| 937 | 18285528 | Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. |
| 938 | 18285528 | Effects of a high-glucose environment on the pituitary growth hormone-releasing hormone receptor: type 1 diabetes compared with in vitro glucotoxicity. |
| 939 | 18285528 | The present study investigated the effects of diabetes and high glucose on GHRH receptor (GHRH-R) mRNA and protein levels in the pituitary of diabetic rats 2, 21, and 60 days post-streptozotocin (post-STZ) administration. |
| 940 | 18285528 | Hypothalamic GHRH mRNA and serum total IGF-I levels were reduced at all three time points. |
| 941 | 18285528 | Membrane lipoperoxidation was present in 33 mM DG, and GHRH-R mRNA levels were diminished after 24 h, Fluo-GHRH internalization was marginal after 16-24 h, and GHRH-induced cAMP levels were decreased after 24 and 48 h. |
| 942 | 18285528 | Altogether, these results indicate that the increase of the 2.5-kb GHRH-R mRNA transcript in vivo could be a consequence of a decrease of hypothalamic GHRH mRNA levels in STZ rats. |
| 943 | 18285528 | Since it does not affect primarily functional GHRH-R levels, the initial diminution of circulating IGF-I levels could result from a decreased GHRH-R stimulation by GHRH. |
| 944 | 19229175 | Here, we demonstrate application of PICUP to cross-linking of three amyloidogenic proteins the 40- and 42-residue amyloid beta-protein variants (Abeta40 and Abeta42), and calcitonin, and a control protein, growth-hormone releasing factor (GRF). |
| 945 | 19332789 | Remarkably, treatment of Br-M3-KO mice with CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br-M3-KO mice by restoring normal pituitary size and normal serum GH and IGF-1 levels. |
| 946 | 19525593 | Neither adrenocorticotropic hormone (ACTH) nor cortisol levels were adequately increased in response to a mixed intravenous administration of corticotropin-releasing hormone, growth hormone-releasing hormone, thyrotropin-releasing hormone and lutenizing hormone-releasing hormone, although other pituitary hormones were increased adequately. |
| 947 | 20087248 | In the last decade new genetic defects have been described in all the levels of the growth hormone-releasing hormone (GH-RH)-GH-IGF (insulin-like growth factor) axis. |
| 948 | 20087248 | Genetic defects in the GHRH and in various parts of the Insulin-like growth factor system have been demonstrated. |
| 949 | 20087248 | In animal models and in humans the importance of the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, TBX19, SOX2 and SOX3 has been extensively studied. |
| 950 | 20087248 | A group of signalling proteins are involved in prenatal (SGA) growth retardation: IRS-1, PDK1, AKT1, and S6K1. |
| 951 | 20087248 | In the last decade new genetic defects have been described in all the levels of the growth hormone-releasing hormone (GH-RH)-GH-IGF (insulin-like growth factor) axis. |
| 952 | 20087248 | Genetic defects in the GHRH and in various parts of the Insulin-like growth factor system have been demonstrated. |
| 953 | 20087248 | In animal models and in humans the importance of the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, TBX19, SOX2 and SOX3 has been extensively studied. |
| 954 | 20087248 | A group of signalling proteins are involved in prenatal (SGA) growth retardation: IRS-1, PDK1, AKT1, and S6K1. |
| 955 | 20379782 | Fasting serum growth hormone (GH): 26.1 ng/mL (0-5 ng/mL), insulin-like growth factor 1 (IGF-1): 635 ng/mL (87-283 ng/mL), GH at 60 min post-ingestion of 75 grams of oral glucose during a glucose tolerance test: 8.3 ng/mL (normal <1 ng/mL). |
| 956 | 20379782 | Postoperatively, serum GHRH, GH and IGF-1 levels fell precipitously. |
| 957 | 20379782 | At 20 months, off octreotide, serum IGF-1 levels had normalized, acromegalic features were receding, and the patient's daily insulin requirements had decreased by 57%. |
| 958 | 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. |
| 959 | 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. |
| 960 | 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. |
| 961 | 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. |
| 962 | 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. |
| 963 | 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. |
| 964 | 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. |
| 965 | 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. |
| 966 | 21777182 | Beside the large family A (rhodopsin-like receptors) and family C GPCR (metabotropic glutamate receptors), the small family B1 GPCR (secretin-like receptors) includes important receptors such as vasoactive intestinal peptide receptors (VPAC), pituitary adenylyl cyclase activating peptide receptor (PAC1R), secretin receptor (SECR), growth hormone releasing factor receptor (GRFR), glucagon receptor (GCGR), glucagon like-peptide 1 and 2 receptors (GLPR), gastric inhibitory peptide receptor (GIPR), parathyroid hormone receptors (PTHR), calcitonin receptors (CTR) and corticotropin-releasing factor receptors (CRFR). |
| 967 | 21825133 | Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas. |
| 968 | 21825133 | Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells. |
| 969 | 21825133 | Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis. |
| 970 | 21825133 | CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells. |
| 971 | 21825133 | Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2. |
| 972 | 21825133 | Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form. |
| 973 | 21825133 | Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus. |
| 974 | 21825133 | Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas. |
| 975 | 21825133 | Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells. |
| 976 | 21825133 | Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis. |
| 977 | 21825133 | CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells. |
| 978 | 21825133 | Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2. |
| 979 | 21825133 | Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form. |
| 980 | 21825133 | Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus. |
| 981 | 21825133 | Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas. |
| 982 | 21825133 | Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells. |
| 983 | 21825133 | Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis. |
| 984 | 21825133 | CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells. |
| 985 | 21825133 | Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2. |
| 986 | 21825133 | Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form. |
| 987 | 21825133 | Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus. |
| 988 | 21825133 | Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas. |
| 989 | 21825133 | Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells. |
| 990 | 21825133 | Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis. |
| 991 | 21825133 | CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells. |
| 992 | 21825133 | Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11β-HSD-1 and up-regulating 11β-HSD-2. |
| 993 | 21825133 | Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11β-HSD-1 enzyme activity or increased 11β-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form. |
| 994 | 21825133 | Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus. |
| 995 | 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). |
| 996 | 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. |
| 997 | 22393012 | Pretreatment with the growth hormone-releasing hormone (GHRH) agonist, JI-36, significantly enhanced graft function by improving glucose tolerance and increasing β-cell insulin reserve in rats thereby allowing for a reduction of the islet mass required for metabolic control. |
| 998 | 23345449 | GHRH receptor is expressed on both adrenal cells and islets. |