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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)
...
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
In this report, we described the clinical, radiographic, and echocardiographic findings in a cat with hypersomatotropism and insulin-resistant diabetes mellitus.
Growth hormone
determinations were made because of persistent hyperglycemia despite insulin requirements exceeding 2.2 U/kg of body weight, and the acromegalic features of the cat. Also, the results of a therapeutic trial in which a long-acting analogue of
somatostatin
was used are discussed.
...
PMID:Hypersomatotropism and insulin-resistant diabetes mellitus in a cat. 291 4
Growth hormone
releasing factors (GRFs) have been isolated from human pancreatic tumours (hGRF) and rat hypothalamus (rhGRF). The response to GRF at the pituitary level can be modulated by other factors, including glucocorticoids, thyroid hormones,
somatostatin
and other neuropeptides and somatomedins. Glucocorticoids enhance GRF-induced growth hormone (GH) secretion in primary cultures of rat anterior pituitary cells, and the synthetic glucocorticoid dexamethasone has recently been shown to increase the amounts of GH released in freely moving rats in response to submaximal doses of intravenous GRF. To investigate whether somatotroph sensitivity to GRF is modulated at its receptor level, we have developed a radioreceptor assay using an iodinated analogue of hGRF as radioligand. We report here that the relative binding affinities of rGRF, hGRF and the two analogues are correlated with their in vitro biological potencies. Further, the number of GRF binding sites is drastically decreased in cells deprived of glucocorticoids either in vivo or in vitro.
...
PMID:Binding sites for growth hormone releasing factor on rat anterior pituitary cells. 298 7
Growth hormone
pulse amplitude is intimately connected with growth in childhood. Its effects are most clear in middle childhood, although the influence of adrenal androgens is probably also important. In infancy, nutrition plays an important part and, in the adolescent growth spurt, the synergism with sex steroids is important. Detailed attention needs now to be focussed on the mechanisms by which growth hormone is secreted and has its action; these include the effects of GHRH,
somatostatin
, insulin and IGF-I.
...
PMID:Growth and growth hormone secretion. 305 53
Growth and lactation are complex processes controlled by several metabolic hormones such as insulin, glucagon, and thyroid hormones but most notably growth hormone.
Growth hormone
secretion is regulated by two hypothalamic hormones,
somatostatin
, an inhibitory regulatory factor, and growth hormone-releasing factor. The quantity and pattern of growth hormone secretion is ultimately regulated in concert by the secretion of both regulatory factors from the hypothalamus through the hypothalamo-hypophyseal portal system, where they exert their actions at unique pituitary receptors. Because the potential use of exogenous growth hormone administration for the stimulation of growth efficiency and lactation has been demonstrated, recent efforts have been directed toward the enhancement of production through manipulation of endogenous growth hormone secretion via its releasing factor. Thus far, releasing factor-stimulated growth and lactation has not been achieved to the same extent as that of exogenous growth hormone. Growth hormone-releasing factor has stimulated growth in two growth hormone-deficient children, as well as female, but not male, rats. Although all food-producing species tested to date respond to growth hormone-releasing factor with the appropriate growth hormone response, continuous or pulsatile administration of releasing factor has not resulted in increased growth rate in sheep, chicks, or hogs. Despite levels of circulating growth hormone that would be expected to produce a 30% increase in milk production if given exogenously to dairy cows, releasing factor-stimulated growth hormone secretion has resulted in only a 3 to 9% increase. It is clear from these studies that further developments are necessary to demonstrate the practical application of growth hormone-releasing factor.
...
PMID:Growth hormone-releasing factor effects on pituitary function, growth, and lactation. 310 44
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.
...
PMID:Nonthyroidal control of metabolism after burn injury: possible role of glucagon. 401 May 24
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.
...
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.
...
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.
...
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.
...
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
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