Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At present, four main types of serotonin (5-HT) receptors have been identified in the brain (5-HT1, 5-HT2, 5-HT3, and 5-HT4). In addition, the 5-HT1 have been further subclassified. We have taken advantage of a new selective 5-HT1D receptor agonist 3-[2-(dimethylamino)ethyl]-N-methyl-1H-indole-5-methanesulfonamide succinate, Sumatriptan, to evaluate the role of 5-HT1D receptors on GH secretion. To this end, several tests with or without sumatriptan were undertaken in normal prepubertal children. Furthermore, we assessed the effect of Sumatriptan on basal GH secretion and the GH response to GHRH in obese children. In normal children, Sumatriptan administration (3 mg, sc) resulted in an increase in basal GH levels at 30 min (7.7 +/- 1.5 micrograms/L; P < 0.05) and increased GH responses to GHRH (47.3 +/- 6.4 vs. 29.6 +/- 9.7 micrograms/L; P < 0.05). The Sumatriptan-induced increase in GH responses to GHRH was dependent on the stimulus tested. Pretreatment with Sumatriptan did not modify the GH response to clonidine or pyridostigmine, as assessed by the peak GH response and the area under the curve. In contrast, it increased the GH response to arginine. In the obese subjects, the GH response to GHRH was reduced (7.3 +/- 1.0 vs. 29.6 +/- 9.7 micrograms/L at 30 min) compared to that in control children (P < 0.05). Sumatriptan administration did not alter the basal GH value (peak GH, 1.7 +/- 0.3 micrograms/L at 30 min). However, Sumatriptan administration clearly increased the effect of GHRH, resulting in a GH peak of 14.6 +/- 3.1 micrograms/L at 30 min (P < 0.01). To assess the specificity of Sumatriptan on anterior pituitary hormone secretion, we studied its effect on TSH and PRL responses to TRH as well as LH-releasing hormone-induced LH and FSH secretion. Administration of Sumatriptan did not alter the response of any of these hormones. Our results indicate that 5-HT1D receptors have a stimulatory effect on GH secretion, possibly by inhibiting hypothalamic somatostatin release.
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PMID:Role of the serotonin receptor subtype 5-HT1D on basal and stimulated growth hormone secretion. 777 48

To assess the possible influence of alcoholism on serotonergic control of growth hormone (GH) secretion, 6 mg of the 5-HT1D serotonergic receptor agonist, sumatriptan, was injected subcutaneously in a group of nine normal controls (aged 32 to 49 years) and in nine age-matched nondepressed male alcoholic subjects after 10 to 25 days of abstinence from alcohol. During the same period, subjects were also tested with GH-releasing hormone ([GHRH] 1 microgram/kg body weight in an intravenous [i.v.] bolus) and L-arginine, which releases GH from somatostatin inhibition (50 g in 50 mL normal saline over 30 minutes) to determine whether GH secretion in response to alternate secretagogues is preserved in alcoholics. A control test with administration of normal saline instead of drug treatments was also performed. Plasma GH levels were recorded over 2 hours in all tests. Administration of placebo did not change plasma GH levels in any subject. Similar GH responses were observed in normal controls and alcoholic subjects when GHRH or arginine were administered. A significant GH increase was observed in normal controls after sumatriptan injection; in contrast, GH secretion was not modified by sumatriptan administration in alcoholic patients. These data show that alcoholism is associated with an impairment in the serotonergic-stimulatory regulation of GH secretion, whereas GH responses to direct pituitary stimulation with GHRH or to release from somatostatinergic inhibition with arginine appear to be preserved in alcoholics.
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PMID:Alcoholism abolishes the growth hormone response to sumatriptan administration in man. 878 27

In order to establish whether long-term abstinence from alcohol reverses the defective serotonergic and GABAergic controls of growth hormone (GH) secretion affecting alcoholic patients, the 5-HT1D serotonergic receptor agonist sumatriptan and the GABAergic agent gamma-hydroxybutyric acid (GHB) were administered to 12 normal men (32-49 years) and 22 non-depressed male alcoholic subjects (38-52 years) after 1-2 years of abstinence from alcohol. All subjects were also tested with placebos. Furthermore, tests with GH-releasing hormone (GHRH) and L-arginine (which releases GH from somatostatin inhibition) were performed to determine whether GH secretion in response to its major determinants is preserved in alcoholics. Administration of placebo did not change plasma GH levels in any subject. Similar GH responses were observed in normal controls and alcoholic subjects when GHRH or arginine were administered. A significant GH increase was observed in normal controls after sumatriptan or GHB injection; in contrast, GH secretion was not modified by sumatriptan or GHB administration in alcoholic patients. These data show a persistent selective loss of 5-HT1D receptor and GHB-mediated neurotransmissions in alcoholics that a long-term abstinence from alcohol is unable to restore.
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PMID:Persistence of defective serotonergic and GABAergic controls of growth hormone secretion in long-term abstinent alcoholics. 913 96

Nitric oxide (NO) is a highly reactive gas that has been suggested to function as a neurotransmitter in the neuroendocrine system. In this work, we have evaluated the role of NO pathways in growth hormone (GH) secretion by assessing the effect of L-arginine infusion, a precursor of NO formation, and L-NAME, a nitric oxide synthase (NOS) inhibitor. The experiments were carried out on 7 adult beagle dogs. A saline infusion was carried out on all the dogs as a control test. L-arginine (infusion i.v. 10 g in 100 ml of saline, from t = 0 to 30 min) and L-nitro-arginine-methyl ester, L-NAME (infusion of 300 microg/kg in 120 ml of saline, from t = -30 to 45 min) were administered alone and together with growth hormone-releasing hormone (GHRH) (i.v. bolus at 0 min, at a dose of 100 microg), the synthetic GH secretagogue GHRP-6 (i.v. bolus at 0 min, at a dose of 90 microg), and the 5-HT1D serotonin receptor agonist sumatriptan, SUM (s.c. injection at the dose of 3 mg). Plasma cGH was determined by RIA. Results were evaluated by one-way analysis of variance, followed by the Newman-Keuls test for multiple comparisons. L-arginine administration resulted in a slight increase in plasma cGH in comparison with saline controls. Combined administration of L-arginine and GHRH enhanced cGH release in comparison with GHRH alone. L-NAME alone did not modify baseline cGH levels, but completely suppressed the GH release induced by GHRH or GHRP-6. It also strongly reduced, but did not abolish the effect of the two peptides (GHRH plus GHRP-6) administered together. Finally, administration of the 5-HT1D agonist SUM induced a significant cGH secretion in all dogs, a response which was not modified when L-NAME was administered in combination with SUM. In conclusion, our data show that inhibition of NO blunts both GHRH or GHRP-6-induced cGH release, and are compatible with the hypothesis that it acts by decreasing hypothalamic somatostatin release.
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PMID:Involvement of nitric oxide in the regulation of growth hormone secretion in dogs. 1159 77