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

Growth hormone (GH) pulses in vivo are associated with increased hypothalamic portal growth hormone releasing hormone (GH-RH) concentration and can be prevented by GH-RH antisera. GH pulses are also associated with prior reduction of portal somatostatin (SRIF) concentrations, although SRIF antisera do not abolish GH pulses. In vitro, pulses of GH-RH as well as SRIF withdrawal are followed by pulses of GH release; the presence of GH-RH enhances post-SRIF GH release. We asked four questions: (1) During combined GHRH-SRIF exposure in vitro, must SRIF withdrawal be complete to produce a pulse of GH release, or is there a threshold diminution of SRIF which permits it? (2) When pulsatile GH release does occur, is it an all-or-none phenomenon, or is it titratable by fractional reduction of SRIF? (3) Does varying the GH-RH concentration while administering SRIF systematically alter GH release in response to fractional SRIF reduction? (4) Given a small but distinct effect of GH-RH on release of stored prolactin (PRL) in this system, does fractional SRIF reduction alter PRL release in parallel? Rat pituitary tissue whose hormone stores had been prelabeled with tritium was perifused for 120 min in combined 25 nM SRIF and 3 or 10 nM rat GH-RH (rGH-RH). Then, while maintaining rGH-RH concentrations, the SRIF concentration was left unchanged (control) or was reduced to 20, 15, 10, 5, or 0 nM for 60 min. Release of stored rGH and rPRL was assessed by immunoprecipitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fractional reduction of somatostatin concentration interacted with rat growth hormone releasing hormone to titrate the magnitude of pulsatile growth hormone and prolactin release in perifusion. 290 14

The inhibitory effect of somatostatin on gastrin release is well known. Could the growth hormone releasing hormone (GHRH), an antagonist of somatostatin on growth hormone (GH) release, have a gastrin-releasing effect on gastrin? To answer this question, two types of experiments were conducted: (1) The study of the effect of GHRH on gastrin in rats, which showed a significant and dose related release for the three doses studied: 0.12, 0.6 and 3.0 micrograms/rat. (2) The study on the recurrence of this gastrin releasing effect which has been found to be significant (1 to 5 injections at 1 hour intervals). Our data suggest that GHRH is an hypothalamic releasing factor for gastrin release. Accordingly, gastrin may mediate the observed proliferative effect of GHRH in the upper digestive tract.
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PMID:Growth hormone releasing hormone stimulates the release of gastrin in rat. 309 93

The hypothalamo-pituitary-gonadotrophic axis develops in the sheep fetus from midgestation to late gestation. The GnRH neuronal centres seem to be fully developed in the fetus and their localization complies with the adult pattern. Pituitary gonadotrophs are responsive to exogenous GnRH and release LH and FSH in a pulsatile fashion; the highest concentrations in plasma are found during late gestation. In sheep, maturational changes of this axis continue through to the prepubertal period. The GnRH neuronal system is established at about 12 weeks of age. The pattern of LH and FSH release is characteristic for each gonadotrophin depending on age and sex. The responsiveness of the gonadotrophs to GnRH increases up to 3 weeks of age. It is concluded that the changes in morphology and physiology of the hypothalamo-pituitary-gonadotrophic axis reflect the progressive maturation of the central mechanisms involved in the control of gonadotrophin secretion throughout fetal and prepubertal growth in sheep. Development of the hypothalamo-pituitary-somatotrophic axis begins in the fetus around mid-gestation. The central regulation of growth hormone (GH) in the fetus probably has a dual character, although the growth hormone releasing hormone (GHRH) neuronal system has not yet been observed in sheep. The somatostatin neuronal system develops in diverse neuronal centres in the fetus. The somatostatin centre involved in hypophysiotrophic functions does not develop fully before birth and is established over the first 10 weeks after birth. Plasma GH concentrations are very high in the fetus and fall suddenly in the perinatal period, and after a temporary increase they decline with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of the gonadotrophic and somatotrophic axes of sheep. 762 13

Pirenzepine, a muscarinic antagonist probably acting via stimulation of hypothalamic somatostatin release, abolishes the growth hormone releasing hormone (GHRH)-stimulated growth hormone (GH) rise in normal subjects but only blunts it in patients with anorexia nervosa (AN). This finding suggested the existence in AN of an alteration of cholinergic system and/or somatostatinergic tone. To further investigate these mechanisms, in 11 AN women patients (age 18.8 +/- 0.9 years; BMI 13.4 +/- 0.4) we studied the GH response alone (1 microgram/Kg IV as a bolus at 0 min) and combined with pyridostigmine (PD, 120 mg orally, 60 min before GHRH administration), a cholinesterase inhibitor, or arginine (ARG 30 g infused over 30 min starting at 0 min), two compounds probably acting via inhibition of hypothalamic somatostatin (SS) release. The GH response to GHRH preceded by a previous (120 min before) neurohormone administration also was studied. All these tests also were performed in 20 normal age-matched women (age 22.0 +/- 1.8 yrs; BMI20.1 +/- 2.4). Basal serum GH levels were higher in AN patients than in normal volunteers (NV) (10.3 +/- 3.4 versus 2.8 +/- 0.3 microgram/L; p < 0.001), whereas plasma IGF-I levels were lower in AN patients than in NV (43.3 +/- 10.6 versus 172.4 +/- 13.9 micrograms/L; p < 0.00001). In AN patients, GHRH administration induced a GH rise higher, though not significantly, than that in NV [delta area under the curve (AUC) 1173.6 +/- 167.6 versus 834.6 +/- 188.1 micrograms/L/h]. The GH response to the second of two consecutive GHRH boluses was lower (p < 0.01) than that of the first one either in AN patients or in NV (67.6 +/- 27.4 and 53.1 +/- 25.7 micrograms/L/h, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine but not pyridostigmine, a cholinesterase inhibitor, enhances the GHRH-induced GH rise in patients with anorexia nervosa. 788 Sep 38

Interleukin-2 (IL-2), which plays a major role in the bidirectional intercellular communication between the neuroendocrine and immune systems, suppressed the release of GH from anterior pituitary halves at femtomolar concentrations. It is well established that the release of GH from the anterior pituitary is regulated by growth hormone releasing hormone (GRH) and growth hormone release-inhibiting hormone (somatostatin). Consequently, we studied the possible effect of IL-2 on the release of somatostatin and GRH from the mediobasal hypothalamus (MBH) in vitro. Single MBHs were incubated with fresh Krebs-Ringer bicarbonate (KRB) buffer alone or KRB containing different concentrations of IL-2 (10(-15)-10(-10) M) for 30 min. After collection of the media, the MBHs were incubated with KRB containing high potassium (high K+ = 56 mM) without IL-2 for a period of 30 min to study the effect of pretreatment with IL-2 on depolarization-induced somatostatin and GRH release. Experiments were also undertaken to study the effect of IL-2 in the presence of high K+ or IL-2 in the presence of DA (60 microM), a potent stimulator of somatostatin and GRH release. The minimal effective dose of IL-2 which significantly stimulated the release of somatostatin was 10(-14) M. Depolarization-induced release of somatostatin was reduced significantly by prior treatment with all the concentrations of IL-2 tested (10(-13)-10(-10) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of interleukin-2 on the release of somatostatin and growth hormone-releasing hormone by mediobasal hypothalamus. 790 32

Cortisol is known to influence growth hormone release probably by modulating somatostatin tone. We examined the effect of metyrapone (the 11 beta-hydroxylase inhibitor) treatment on growth hormone response to growth hormone releasing hormone (1 microgram kg-1 body wt). Six healthy male subjects were tested on two occasions 1 wk apart. On one occasion they received metyrapone followed by growth hormone releasing hormone and on the other placebo followed by growth hormone releasing hormone. In all subjects metyrapone produced a significant drop in cortisol levels. Together with this drop there was a significant enhancement of growth hormone response to growth hormone releasing hormone. The GH response was negatively correlated with the cortisol level. Growth hormone release in response to growth hormone releasing hormone challenge is thus seen to be heavily influenced by cortisol levels.
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PMID:Lowering cortisol enhances growth hormone response to growth hormone releasing hormone in healthy subjects. 797 13

Medullary thyroid carcinoma (MTC) can be important for gastroenterologists because 20-30% of patients with MTC suffer from chronic diarrhea and the tumor is capable of producing--besides other bioactive substances--a multitude of gastroenteropancreatic hormones. Gastrointestinal hormone profiles of 5 patients with MTC were determined both basally and after intravenous stimulation with secretin and calcium respectively. Diagnosis of MTC was confirmed histologically or cytologically and by demonstration of elevated serum concentration of calcitonin both basally and after calcium stimulation. 4/5 patients had chronic diarrhea. Normal values or only borderline increases were found for the following hormones: vasoactive intestinal polypeptide (VIP), neurotensin, substance P, growth hormone releasing hormone (GRH), glucagon, neurokinin A, peptide YY, and pancreatic polypeptide. Somatostatin was elevated after calcium stimulation in 1/5 patients only. The main findings were increased basal concentrations for GAWK in 5/5 patients and elevated concentrations for gastrin-releasing peptide (GRP, human bombesin) after calcium stimulation in 4/5. Probably as a consequence of the GRP increase, an increase in gastrin occurred in parallel, indicating bioactivity of the GRP released from the tumor. Besides calcitonin as the main tumor marker for MTC, determination of GAWK and GRP seems to provide helpful additional markers in laboratory diagnosis of MTC. GRP determination after i.v. calcium infusion allowed identification of patients with normal basal plasma GRP concentration.
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PMID:[Gastrointestinal hormone profile in medullary thyroid carcinoma]. 801 6

An acquired defect in growth hormone secretion in mature dogs has been associated with some forms of generalised alopecia. In an attempt to elucidate the pathogenesis of the disturbance in growth hormone release, the plasma concentrations of growth hormone and insulin-like growth factor I (IGF-I) were measured in two seven-year-old poodles with alopecia and, for comparison, in two young German sheperd dogs with congenital hyposomatotropism (pituitary dwarfism). In the poodles the basal concentrations of growth hormone were low, although often above the detection limit of the assay. The concentrations of IGF-I were in the reference range for healthy poodles. No growth hormone could be detected in the plasma of the German sheperd dogs and the concentrations of IGF-I were very low. Stimulation with clonidine and growth hormone releasing hormone (GHRH) before and after repeated injections of GHRH did not result in significant increases in growth hormone concentrations in plasma. The concentrations of growth hormone in the poodles fluctuated at low levels during the test period. In the German sheperd dogs the levels of growth hormone remained unmeasurable during the stimulation tests. It was concluded that in the two poodles the basal concentrations of growth hormone were sufficient to maintain normal IGF-I concentrations, and thus the release of growth hormone was considered appropriate. Based upon measurements of urinary corticoids and a review of the literature it is suggested that the lack of a growth hormone response to stimulation was due to the enhanced release of somatostatin as a result of mild and fluctuating hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbed release of growth hormone in mature dogs: a comparison with congenital growth hormone deficiency. 811 57

The concentration of extracellular calcium rightly regulates calcitonin secretion by calcium influx through dihydropyridine-sensitive voltage-dependent calcium channels; the result is an increase in intracellular calcium. There also exists a cAMP-dependent pathway of calcitonin release activated by glucagon or growth hormone releasing hormone. In thyroid C-cells, as in all cells, there is dual regulation of adenylate cyclase, mediated by inhibitory or stimulatory G proteins; glucagon stimulated cAMP production can be inhibited by somatostatin via pertussis toxin sensitive inhibitory G proteins. Somatostatin inhibits not only cAMP dependent but also calcium-dependent calcitonin secretion. Furthermore, somatostatin inhibits voltage dependent calcium channel currents thereby lowering cytosolic calcium. These actions also involve a pertussis toxin-sensitive inhibitory G protein but they occur independently of changes in the cytosolic cAMP concentration. Thus multiple interactions between second messenger systems at different cellular levels modulate calcitonin secretion.
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PMID:Regulation of calcitonin secretion in vitro. 822

To study the site of lesions in idiopathic growth hormone (GH) deficiency (IGHD), growth hormone releasing hormone (GHRH) was administered sequentially for 3 days to 19 patients with IGHD, 3 patients with GH deficiency (GHD) secondary to hypothalamic tumors, and 7 normal short children (NSC). GHRH (100 micrograms) was injected as a bolus on days 1 and 3, and was infused over 60 min on day 2. Of 19 patients with IGHD, 6 showed an improved GH response (group A), 5 a decreased response (group B) and the remaining 8 an unchanged response (group C) to sequential administration of GHRH. The response was unchanged in patients with secondary GHD or NSC. There was no significant correlation between the patterns of GH response and the findings on pituitary MR images or the delivery state at birth in IGHD patients. Ten patients with IGHD (4 of group A; 3 each of groups B & C) and 2 NSC showed much greater GH responses to arginine (0.5 g/kg i.v. for 30 min) injected with preceding GHRH than to arginine injected without preceding GHRH. These results indicate that hypothalamic lesions were primarily responsible for GH deficiency in about 60% of the patients with IGHD (groups A and B), and group C might have more severe hypothalamo-pituitary damages than the other groups. Hypothalamic somatostatin neurons seems to be functioning to a degree even in severe IGHD patients.
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PMID:Plasma GH response to the sequential 3 day administrations of GHRH followed by arginine infusion in patients with idiopathic GH deficiency and normal short children. 823 47


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