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-releasing hormone was isolated 1982 from human pancreatic tumours. They were found to consist of three peptides (GHRH1-44, GHRH1-40, GHRH1-37) which in vivo and in vitro were specific stimulators of pituitary growth hormone secretion. These tumor-derived GHRHs were demonstrated to be identical to human hypothalamic GHRHs. Extrahypothalamic GHRH is present in some brain regions and in the gastrointestinal tract. Circulating GHRH is detectable in human plasma, but little is known about its function. Above all binding of GHRH to a specific receptor stimulates growth hormone secretion through formation of cyclic AMP. GHRH secretion is modulated by somatostatin, the somatomedins and growth hormone itself. Following single injection of GHRH1-44 i.v. the equilibration half-time is 1.0 +/- 0.2 min and elimination half-time is 6.8 +/- 1.2 min. Maximal growth hormone response is achieved after injection of 1 microgram/kg GHRH. Using higher GHRH-doses growth hormone can be stimulated via subcutaneous or intranasal application. A single i.v. GHRH-test is not sufficient to prove a pituitary defect since growth hormone can be stimulated following repetitive injections in some cases. About 50% of patients with growth hormone deficiency have a hypothalamic defect of GHRH release. In some of these patients GHRH s.c. can promote linear growth to the same degree as growth hormone treatment.
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PMID:[Growth hormone releasing hormone. Review]. 313 22

A female patient with acromegaly, hypercalcemia, and Zollinger-Ellison syndrome was found to have a very high plasma concentration (average 2,300 pmol/liter; normal less than 50 pmol/liter) of growth hormone-releasing factor as measured by a radioimmunoassay to human pituitary growth hormone-releasing factor-1-44. The plasma concentration of growth hormone averaged 25 mIU/liter (normal less than 5 mIU/liter) and there was no rise following an intravenous 100 micrograms bolus of human pituitary growth hormone-releasing factor-1-44. Plasma growth hormone and growth hormone-releasing factor levels were unaffected by bromocriptine, insulin-induced hypoglycemia, and sleep. A long-acting somatostatin analogue lowered both the growth hormone-releasing factor and the growth hormone levels. Thyrotropin-releasing hormone stimulation and oral glucose tolerance tests produced significant increases in plasma growth hormone levels whereas the growth hormone-releasing factor level remained unchanged, suggesting that when normal somatotrophs are exposed to maximal growth hormone-releasing factor stimulation, thyrotropin-releasing hormone becomes a secretagogue of growth hormone from the pituitary. It is proposed that in the absence of a radioimmunoassay for growth hormone-releasing factor, a lack of growth hormone response to growth hormone-releasing factor in a patient with acromegaly is compatible with a source of ectopic growth hormone-releasing factor production.
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PMID:Growth hormone secretion dynamics in a patient with ectopic growth hormone-releasing factor production. 392 80

The effects of iontophoretically applied human pancreatic growth hormone-releasing factor (hpGRF), peptide histidine isoleucine (PHI-27), and somatostatin (SS) on the extracellular activity of single cells in the hypothalamus, thalamus, and cortex of the rat brain were studied in urethane-anesthetized, male rats. Neurons with membrane sensitivity to hpGRF, PHI-27, and SS were present in each brain region. Although neurons excited by these peptides were encountered in thalamus and hypothalamus, depression of neuronal firing was the predominant response observed. Overall, the neurons responding to hpGRF also possessed membrane sensitivity to PHI-27, whereas, the hpGRF sensitive neurons appeared to be more divided as to their ability to respond to SS. The results clearly demonstrate that hpGRF and PHI-27 are capable of affecting the membrane excitability of neurons in several brain regions. The distribution of neurons sensitive to hpGRF suggests that hypothalamic GRF, in addition to its well documented role in the regulation of pituitary growth hormone secretion, may subserve other physiological events in the rat central nervous system as a neurotransmitter and/or neuromodulator.
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PMID:Sensitivity of rat forebrain neurons to growth hormone-releasing hormone. 393 50

The endocrine basis for control of metabolism in nonthyroidal illness is not yet understood. Burn injury is associated with reduced serum concentrations of thyroid hormones and with resting hypermetabolism. One index of severity is total burn size (TBS, % body surface). After overnight fasting and recumbency, resting metabolic rate (MR, O2 consumption) was measured weekly and plasma was sampled for determination of glucose, total cholesterol, triglycerides, insulin, glucagon, somatostatin, growth hormone, norepinephrine, epinephrine, and cortisol in 28 burned men, 17-23 years old, TBS 2%-85%, including 8 controls with minimal injury (TBS less than or equal to 7.5%). MR was elevated in proportion to burn size mainly in the first week then declined toward normal. Growth hormone was not changed. Two multiple regression analyses (validated by random partitioning of data) determined which plasma variables independently reflected residual variation in MR: without TBS entered as a variable, high MR was associated with elevated glucose, cortisol, and glucagon, and low cholesterol (cumulative r2 = 0.79); with TBS entered, high MR was associated with greater TBS, elevated norepinephrine, and again high glucagon and low cholesterol (r2 = 0.81). Resting metabolism after burn injury is controlled not by the thyroid but may be controlled by a set of antiinsulin hormones that does not include growth hormone, but possibly includes glucagon.
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PMID:Nonthyroidal control of metabolism after burn injury: possible role of glucagon. 401 May 24

Somatostatin, a hypothalamic peptide that inhibits the secretion of pituitary growth hormone, inhibits basal insulin secretion in fasted cats and rats. In fasted baboons both basal and arginine-stimulated secretion of insulin and glucagon are inhibited. Somatostatin appears to act directly on the endocrine pancreas. The action is dose-related, rapid in onset, and readily reversed.
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PMID:Somatostatin: hypothalamic inhibitor of the endocrine pancreas. 459 11

Growth hormone (GH) release from Rat pituitary cell monolayers in response to synthetic somatocrinin (7.8 to 1,000 pmol/l) is paralleled with an increase in cellular cyclic AMP (cAMP) content and efflux of cAMP in the extracellular medium. Somatostatin and blockers of calcium-dependent cellular mechanisms inhibit somatocrinin-induced GH release but only partially decrease (somatostatin, CoCl2) or even increase (trifluoperazine) cAMP levels. Thus, calcium is required for somatocrinin action and GH release is not simply dependent on stimulation of cAMP metabolism.
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PMID:[Roles of cyclic AMP and calcium in the mechanism of the release of growth hormone by somatocrinin]. 609 53

Pituitary growth hormone (GH) secretion is regulated by two hypothalamic factors: somatostatin, a characterized tetradecapeptide, which inhibits secretion, and GH-releasing factor, unidentified, which stimulates secretion. Biogenic amines, including norepinephrine, dopamine, serotonin, acetylcholine, and gamma-aminobutyric acid have excitatory or inhibitory effects at brain sites to modulate hypothalamic control. alpha-Adrenergic mechanisms have been shown to be of particular importance in the regulation of physiologic GH secretion, which is characterized by episodic surges of release.
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PMID:Functions of central nervous system neurotransmitters in regulation of growth hormone secretion. 610 74

Five insulin treated diabetics were studied on three consecutive days. Overnight variable intravenous insulin infusions were used before each study to maintain normoglycaemia and to calculate the optimal basal insulin infusion rate (1.1 +/- 0.1 U/h) which ws then kept constant throughout the study day. A standard 400 kCal breakfast with 25 g xylose was given at 0800 h. When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). Peak post-prandial blood glucose values were similar on all three days. The blood glucose rebounded after the cessation of the somatostatin infusion on day som. Post-prandial blood xylose peaks were lowered by somatostatin on both days but rebounded after the cessation of the somatostatin infusion on day som. The area under the plasma and urinary xylose curves was lowered by somatostatin only on day SOM. Growth hormone and glucagon levels were not statistically different on all 3 days. Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled.
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PMID:Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system. 611 91

Growth hormone (GH) and prolactin (Prl) secretion by a normal human pituitary in dispersed cell culture has been investigated. Prl secretion was significantly stimulated after 0.5, 1, 2 and 4 h exposure to 1, 10, 100 and 1000 ng/ml thyrotrophin releasing hormone (TRH). Maximal effects were obtained with 10 ng/ml TRH at 2 h, higher doses being less effective. GH secretion was unchanged with the exception that 1 ng/ml TRH produced a small decrease at 4 h. GH and Prl secretion was significantly inhibited by incubation with 0.01, 0.1, 1 or 10 micrograms/ml 2-bromo-alpha-ergocryptine (bromocriptine). The inhibition persisted for a further 24 h after removal of bromocriptine. Theophylline (10(-2) M) significantly increased GH and Prl secretion during a 4 h incubation and this effect was blocked by co-incubation with 10 ng/ml somatostatin (SRIF). SRIF also inhibited basal GH and Prl secretion during 4 h and removal of SRIF and incubation for at further 4 h led to a rebound in GH and Prl secretion to levels greater than control. It is concluded that cell culture techniques previously applied to the study of hormone secretion by pituitary adenomas can be equally applied to the normal human pituitary.
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PMID:Growth hormone and prolactin secretion by dispersed cell cultures of a normal human pituitary: effects of thyrotrophin releasing hormone, theophylline, somatostatin, and 2-bromo-alpha-ergocryptine. 611 69

1. Growth hormone secretion, exchangeable cellular sodium and calcium concentrations measured by 22Na and 45Ca incorporation, and efflux of 45Ca were studied in dispersed bovine anterior pituitary cells. 2. Addition of veratridine (100 microM), an activator of sodium channels, increased exchangeable sodium and calcium concentrations in the cells, the efflux of 45Ca from prelabelled cells, and caused a biphasic stimulation of the rate of growth hormone secretion. Secretion of growth hormone was not stimulated when the extracellular calcium was decreased below 0.1 mM. 3. The increases in growth hormone secretion, exchangeable calcium concentration and 45Ca efflux from prelabelled cells caused by veratridine were abolished by addition of the calcium antagonist verapamil (20 microM). Verapamil also reduced the rise in exchangeable sodium caused by veratridine and increased the resting exchangeable sodium concentrations. 4. The peptide somatostatin (1 micrograms/ml) prevented veratridine-stimulated growth hormone secretion but did not inhibit the increases in exchangeable sodium and calcium caused by veratridine. The peptide itself elicited a transient increase in 45Ca efflux and subsequently partially inhibited veratridine-stimulated 45Ca efflux. 5. The data suggest that anterior pituitary cells possess voltage-sensitive sodium channels. Activation of these channels by veratridine may lead to depolarization and increased entry of calcium via potential-dependent calcium channels, which contributes to a rise in cytoplasmic calcium concentration and the subsequent stimulation of growth hormone secretion. We conclude that the calcium antagonist verapamil may also interact with sodium channels, and that the peptide somatostatin may act on growth-hormone-secreting cells either to prevent the rise in cytoplasmic calcium by hyperpolarizing the cells or to decrease the affinity of a population of calcium binding sites in the cells.
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PMID:Inhibition by somatostatin of bovine growth hormone secretion following sodium channel activation. 611 62


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