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PMID |
Sentence |
1 |
22024993
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This review summarizes our current understanding of the role of gonadotropin-releasing hormone (GnRH)/GnRH receptor (GnRHR) signaling at the maternal-fetal interface.
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2 |
707005
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Failure of growth hormone (hGH), cortisol and prolactin to respond to insulin induced hypoglycaemia (0.1 U/kg), of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to respond to gonadotrophin releasing hormone (GnRH, 100 microgram) and of thyrotrophin (TSH) and prolactin to increase after thyrotrophin releasing hormone (TRH, 500 microgram), confirmed the diagnosis of panhypopituitarism.
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3 |
2111887
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GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals.
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4 |
8333840
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In contrast, GnRH and TPA stimulated activin, and to a lesser degree, inhibin production; significantly, this is the first demonstration of activin dimer production by granulosa cells.
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5 |
7826593
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Similarly, pituitary function as assessed by basal gonadotrophins and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release appears to be normal in young women with IDDM.
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6 |
7554320
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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.
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7 |
7674023
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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.
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8 |
12959992
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To test whether the increased incidence of diabetes in castrated male NOD mice is related to an increase in GnRH activity, we treated castrated male NOD mice with Antide, a GnRH receptor antagonist, to determine the effect on the incidence and timing of onset of diabetes.
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9 |
20008557
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Oscillatory synthesis and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH), is essential for normal reproductive development and fertility.
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10 |
20008557
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In contrast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimulated at low rather than high frequencies of pulsatile GnRH.
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11 |
20008557
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We hypothesized that high GnRH pulse frequencies might stimulate a transcriptional repressor(s) to attenuate the action of CRE binding protein (CREB) and show that inducible cAMP early repressor (ICER) fulfills such a role.
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12 |
20008557
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ICER was not detected under basal conditions, but pulsatile GnRH stimulated ICER to a greater extent at high than at low pulse frequencies.
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13 |
20008557
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ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogates both maximal GnRH stimulation and GnRH pulse frequency-dependent effects on FSH beta transcription.
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14 |
20008557
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These data suggest that ICER production antagonizes the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, thereby playing a critical role in regulating cyclic reproductive function.
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15 |
21183781
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Leptin exerts a permissive action on puberty by stimulating release of gonadotropin-releasing hormone (GnRH) in the hypothalamus.
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16 |
21183781
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The Kiss1 gene produces kisspeptins that stimulate GnRH secretion.
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17 |
21076077
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In mouse LbetaT2 immortalized gonadotrophs, rosiglitazone treatment inhibited GnRH stimulation of the stress kinases p38MAPK and MAPKs/JNKs, but did not alter activation of ERKs, both in the presence and absence of activin.
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