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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Growth hormone (GH) secretion was studied in children after a single small intravenous (i.v.) dose of somatostatin (Somatotropin Release Inhibiting Factor, SRIF). After a short decrease of the GH level there was a slow increase culminating at 60 minutes, then again a decrease with the lowest point at 90 minutes. During the third hour the GH level showed a second peak; this was more frequent than the first one. It is concluded that a single small dose of somatostatin during the third hour after its administration can cause an increase of the GH level.
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PMID:Changes of the growth hormone level after a single small dose of somatostatin. 613 27

The effect of physiological elevation of growth hormone levels on ketone body kinetics was determined using a 14C-ketone body tracer technique in normal and acutely insulin-deficient man. Changes of ketone body production and metabolic clearance rates during growth hormone infusion (plasma levels of approximately 25 micrograms/1) were measured during basal conditions and during heparin-induced elevation of non-esterified fatty acid levels. Growth hormone administration to six subjects fasted overnight resulted in an increase in ketone body production which exceeded that observed in nine control subjects (5.5 +/- 0.5 versus 3.1 +/- 0.1 mumol X kg-1 X min-1, p less than 0.025) after elevation of plasma non-esterified fatty acids. Growth hormone infusion increased glycerol and non-esterified fatty acid concentrations indicating enhanced lipolysis. During somatostatin-induced acute insulin deficiency (n = 7), growth hormone enhanced the increase in total ketone body production observed in six subjects receiving somatostatin alone (8.4 +/- 0.8 versus 4.1 +/- 0.7 mumol X kg-1 X min-1, p less than 0.01). Total ketone body metabolic clearance decreased by 50% during somatostatin and remained uninfluenced by growth hormone. Non-esterified fatty acids and glycerol levels increased during somatostatin, and growth hormone failed to alter non-esterified fatty acid levels significantly. The results demonstrate a stimulatory effect of high physiological growth hormone levels on ketogenesis which is largely explained by an enhancement of lipolysis and thus increase in substrate supply for ketogenesis. Growth hormone administration during acute insulin deficiency enhanced ketogenesis in the absence of alterations in plasma non-esterified fatty acid levels, suggesting a direct hepatic ketogenic effect.
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PMID:Effect of physiological elevation of plasma growth hormone levels on ketone body kinetics and lipolysis in normal and acutely insulin-deficient man. 614 2

Somatostatin is a14-amino acid peptide hormone that inhibits the secretion of a variety of other polypeptide hormones, including growth hormone. Here we describe an experimental system used to determine whether somatostatin can discriminate in its inhibition between secretory and plasma membrane proteins. Growth hormone-secreting cells (GH3) were infected with vesicular stomatitis virus and pulse-chased with [35S]methionine to follow the simultaneous intracellular transit of growth hormone and the viral membrane glycoprotein, G protein. Secretion of growth hormone was monitored by immunoprecipitation of chase media, while appearance of G protein on the plasma membrane was detected by cell surface labeling and virus purification. In the presence of somatostatin (10 micrograms/ml), the secretion of growth hormone was inhibited by 80%. In contrast, G protein appeared on the plasma membrane with slightly enhanced kinetics. When cells were treated with the ionophore monensin (0.2 microM), there was a dramatic inhibition of both the secretion of growth hormone and the incorporation of G protein into plasma membranes. Our results on the differential effect of somatostatin provide evidence for sorting of secretory and membrane proteins into distinct compartments in the secretory pathway. The data further suggest that this sorting event occurs late in the Golgi complex or after proteins exit from that organelle.
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PMID:Somatostatin discriminates between the intracellular pathways of secretory and membrane proteins. 614 20

Growth hormone (GH) secreting cells direct complement-mediated plaque formation (clear zones of hemolysis surrounding the somatotropes) in mixed pituitary cell cultures incubated as a monolayer with protein-A coupled ovine erythrocytes (oRBC) in the presence of GH antiserum. Plaques were maximal in number after 4 h; growth hormone-releasing hormone (GHRH) and somatostatin increased and decreased, respectively, the rate of formation of plaques and their final sizes. Approximately 30% of all pituitary cells formed GH plaques and a similar fraction stained for GH using peroxidase-antiperoxidase immunocytochemistry (ICC). The plaque areas of individual somatotropes (reflecting the amount of GH released) covered a 20-fold range from the smallest to the largest in the 3 treatment groups. Somatostatin-treated and untreated cells formed frequency distributions of plaque sizes that were unimodal. In contrast, GHRH produced a bimodal frequency distribution suggestive of a sub-population of somatotropes preferentially responsive to this secretagogue. This new assay coupled with other morphological and biochemical techniques that can be applied to single cells will permit further analysis of these sub-populations of somatotropes.
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PMID:A reverse hemolytic plaque assay for microscopic visualization of growth hormone release from individual cells: evidence for somatotrope heterogeneity. 615 Nov 29

Growth hormone (GH) is a protein hormone produced by the somatotrophs of the anterior pituitary gland of birds and other vertebrates. The secretion of GH in birds is under hypothalamic control; it involves three peptidergic releasing factors: growth hormone-releasing factor (GRF) (stimulatory); thyrotropin-releasing hormone (TRH) (stimulatory); and somatostatin (SRIF) (inhibitory). In addition, there is evidence for effects of biogenic amines (including serotonin and norepinephrine) and prostaglandins at the level of the hypothalamus and possibly also the pituitary gland. In all avian species examined, plasma concentrations of GH are high in young posthatching chicks but low in the adult and embryo. The difference in plasma concentrations of GH between young and adult birds is due to both greater GH secretion and reduced clearance. The lower secretion of GH in adult birds reflects fewer somatotrophs in the pituitary, changes in somatotroph structure, and reduced GH responses to TRH or GRF administration. There is only limited data on the role of GH in birds. GH appears to be required for normal growth; acting at least in part by increasing somatomedin production. However, plasma concentrations of GH do not necessarily correlate with growth rate. For instance, in chicks with reduced growth rate owing to either goitrogen or protein deficiency in the diet, plasma concentrations of GH are elevated. GH also can influence lipid metabolism by increasing lipolysis, decreasing lipogenesis, and stimulating the uptake of glucose by adipose tissue. The physiological significance of these actions is, however, not established. In addition, GH affects the secretion of other hormones, the immune system, and perhaps also the reproductive system.
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PMID:Growth hormone: its physiology and control. 615 79

Growth hormone (GH)-releasing activity has been detected in extracts of carcinoid and pancreatic islet tumors from three patients with GH-secreting pituitary tumors and acromegaly. Bioactivity was demonstrated in 2 N acetic acid extracts of the tumors using dispersed rat adenohypophyseal cells in primary monolayer culture and a rat anterior pituitary perifusion system. The GH-releasing effect was dose responsive and the greatest activity was present in the pancreatic islet tumor. Small amounts of activity were also found in two other tumors (carcinoid and small cell carcinoma of lung) unassociated with GH hypersecretion. Each of the tumors contained somatostatin-like immunoreactivity but the levels did not correlate with the net biologic expression of the tumor. Sephadex G-75 gel filtration indicated the GH-releasing activity to have an apparent molecular size of slightly greater than 6,000 daltons. The GH-releasing activity was adsorbed onto DEAE-cellulose at neutral pH and low ionic strength, from which it could be eluted by increasing ionic strength. The GH-releasing activity was further purified by high pressure liquid chromatography using an acetonitrile gradient on a cyanopropyl column to yield a preparation that was active at 40 ng protein/ml. Partially purified GH-releasing activity, from which most of the bioactive somatostatin had been removed, increased GH release by pituitary monolayer cultures to five times base line. Enzymatic hydrolysis studies revealed that the GH-releasing activity was resistant to carboxypeptidase, leucine-aminopeptidase, and pyroglutamate-amino-peptidase but was destroyed by trypsin and chymotrypsin, indicating that internal lysine and/or arginine and aromatic amino acid residues are required for biologic activity and that the NH2-terminus and CO9H-terminus are either blocked or not essential. The results provide an explanation for the presence of GH-secreting tumors in some patients with the multiple endocrine neoplasia syndrome, type I, and warrant the addition of GH-releasing activity to the growing list of hormones secreted by tumors of amine precursor uptake and decarboxylation cell types.
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PMID:Partial purification and characterization of a peptide with growth hormone-releasing activity from extrapituitary tumors in patients with acromegaly. 624 40

Growth hormone-secreting human pituitary adenoma cells in long-term culture show a decline in GH secretion. We investigated the effects of dexamethasone on GH production and on the responsiveness of the adenoma cells to various drugs. Twenty-four-hour GH secretion by cultures from seven acromegalics was consistently stimulated by 100 nM-dexamethasone. In four out of seven cultures the effect of dexamethasone occurred within 24 h. After 3 weeks in culture the decline in GH secretion by control cultures was over 90%, while in dexamethasone-treated cultures this was limited to less than 50%. The effect of dexamethasone was dose-dependent over a range of 1 nmol/l to 10 mumol/l. Dexamethasone stimulated not only GH secretion (fivefold), but also GH content (twofold). Cycloheximide and actinomycin D blocked the stimulatory effect of dexamethasone on GH secretion, the latter irreversibly. After 4 days of treatment with 100 nM-dexamethasone, the relative effects of somatostatin, prostaglandin E1, bromocriptine and thyrotrophin releasing hormone were the same in treated and untreated cultures. However, the response to synthetic GH releasing factor (GRF) was greatly enhanced by pretreatment of adenoma cells with dexamethasone (100 and 5 nmol/l). Cells unresponsive to small concentrations of GRF could be stimulated effectively by GRF after pretreatment with dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human growth hormone-secreting pituitary adenoma cells in long-term culture: effects of dexamethasone and growth hormone releasing factor. 642 77

Growth hormone (GH) participates in the regulation of its own secretion by acting through a short-loop feedback mechanism to regulate the synthesis and secretion of somatostatin (SS) and growth hormone-releasing hormone (GHRH). The mechanism of GH's action in certain peripheral targets involves the induction of c-fos. Similarly, we hypothesized that GH induces the expression of c-fos mRNA in SS and GHRH neurons in the hypothalamus. Using in situ hybridization, we observed a significant induction of c-fos mRNA in the arcuate nucleus of human GH-treated compared with control animals. Contrary to our hypothesis, only 11% of GHRH mRNA-containing and 5% of SS mRNA-containing neurons colabeled for c-fos mRNA. These findings indicate that GH feedback on the hypothalamus includes the induction of c-fos mRNA primarily in neurons other than GHRH and SS in the arcuate nucleus and suggest that these unidentified neurons located in the arcuate nucleus are directly involved in transducing the effects of GH in the brain.
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PMID:Identification of target cells for growth hormone's action in the arcuate nucleus. 748 86

Growth hormone secretion is mainly regulated by the interplay of GHRH and somatostatin, two specific hypophysiotrophic neurohormones. In addition to GHRH and somatostatin, many neurotransmitters and neuropeptides influence GH secretion mainly by acting at the hypothalamic level. This paper focuses on the stimulatory role of acetylcholine, arginine and galanin as well as on the inhibitory influence of catecholamines which is mediated by the activation of beta-adrenergic receptors. Attention will be given to the age-related changes in the neural control of GH secretion from childhood to old age.
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PMID:Neurotransmitter control of growth hormone secretion in humans. 752 25


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