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)

The effects of a synthetically obtained mixture of amino acids (FACE) were investigated on the trophic and neurosecretory activity of in vitro cultures of fetal rat neuronal cells. The addition of 10(-6) M FACE to the culture medium significantly increased cell DNA content. Secretions of IR-SRIF, IR-VIP, and IR-GRF were also augmented in different proportions by the presence of FACE. Time studies demonstrated that IR-SRIF was significantly increased after 48 (P less than 0.05) and 72 (P less than 0.01) hr of exposure to FACE, and IR-VIP secretion was potentiated after only 24 hr of culture. Dose-response experiments with 10(-7) to 10(-4) M FACE indicated that concentrations of 10(-5) and 10(-4) M significantly increased both somatostatin released to the medium and cell content of IR-SRIF. FACE concentrations as low as 10(-10) M augmented the secretion of IR-GRF, and there was a dose-response correlation between 10(-10) and 10(-5) M FACE. The release and cell content of IR-VIP were also increased by FACE, with a dose-response relation at concentrations of 10(-9) to 10(-6) M. It can thus be concluded that FACE has a powerful effect on the multiplication and survival of fetal cerebrocortical cells and is also an important potentiator of IR-SRIF, IR-VIP, and IR-GRF secretion.
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PMID:Neurosecretory and trophic action on fetal rat neuroblasts induced by an amino acid mixture. 196 52

Somatostatin pretreatment sensitizes rat anterior pituitary to hGRF stimulation in vitro. The pretreatment (1 nM for 10 min) facilitated GH release response of dispersed rat anterior pituitary cells to hGRF (1 nM for 3 min) 2.04-fold in a perifusion system. The effect lasted even 20 min after the pretreatment. SRIF pretreatment decreased cAMP content in the cells after hGRF stimulation to 61% of the control value. When hGRF was replaced by 1 mM DBcAMP and 15 mM KCl, the pretreatment increased GH secretion 1.69- and 1.67-fold respectively. SRIF pretreatment (1 nM for 10 min) caused a larger increase in (Ca2+)i by hGRF than that of control. The effect of SRIF pretreatment facilitates GRF-induced increase in GH secretion probably through the stimulation of increase in (Ca2+)i.
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PMID:Somatostatin pretreatment facilitates GRF-induced GH release and increase in free calcium in pituitary cells. 197 87

The purpose of this study was to investigate the precise mechanism by which central alpha 2-adrenergic pathways modulate GH secretion in humans. In 10 normal subjects we compared the pattern of clonidine-induced GH release to that elicited by GH-releasing hormone (GHRH) given at a time of presumably similar responsiveness of the somatotrope. We also evaluated the effect of stimulation by GHRH (either endogenous, by administration of clonidine, or exogenous) on the GH response to a further exogenous GHRH stimulation. In 2 experiments the administration of clonidine (0.150 mg, orally) at 0 or 60 min was followed by a GHRH [GRF-(1-29); 1 micrograms/kg, iv] challenge at 180 min. In other experiments subjects received on separate occasions placebo or clonidine at 0 min, followed by GHRH at 60 min and again at 180 min. In a further experiment the administration of clonidine at 0 min was followed by 2 GHRH challenges (60 and 180 min later). The administration of clonidine 60 or 120 min, but not 180 min, before the GHRH bolus significantly (P less than 0.01) increased the GH responses to this challenge compared to those elicited by GHRH when given after placebo in a period of a similar somatotrope responsiveness. These, in turn, were significantly (P less than 0.05) higher than those elicited by clonidine alone. The close relationship between pre-GHRH plasma GH values and GHRH-elicited GH peaks, not observed for clonidine, was lost after pretreatment with this drug. These data indicate that clonidine was able to disrupt the intrinsic hypothalamic-somatotroph rhythm, suggesting that alpha 2-adrenergic pathways have a major inhibitory effect on somatostatin release. Our data also indicate that GH responses to a GHRH bolus administered 120 min after a prior GHRH challenge are dependent on two parameters: the intrinsic hypothalamic-somatotroph rhythm at the time of the second GHRH bolus, and the magnitude of GH secretion elicited by the previous somatotroph stimulation. In summary, alpha 2-adrenergic agonism appears to act primarily in GH control by inhibiting the hypothalamic release of somatostatin, rather than by stimulating GHRH secretion.
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PMID:Alpha 2-adrenergic agonism enhances the growth hormone (GH) response to GH-releasing hormone through an inhibition of hypothalamic somatostatin release in normal men. 197 61

The effect of electrical stimulation of the hypothalamic periventricular nucleus (PVN) on plasma GH profile was studied in unanesthetized female Wistar rats. A bipolar concentric electrode was implanted into the PVN, hypothalamic ventromedial nucleus (VMH), or intervening area between the PVN and VMH. Serial blood specimens were collected from an indwelling right atrial cannula. Plasma GH levels were reduced significantly during electrical stimulation of PVN, and a large rise of plasma GH levels followed after cessation of stimulation. An identical plasma GH profile was observed in response to the repeated stimulation. This rebound secretion of GH was completely inhibited by the administration of rat GRF antiserum. The effect of electrical stimulation of VMH on plasma GH levels was similar to that of PVN stimulation. However, the stimulation of hypothalamic area intervening between PVN and VMH was not followed by a surge of GH secretion. Since a continuous exposure of somatotrophs to GRF even in a concurrent presence of somatostatin (SS) is known to induce attenuation of the GH response to GRF through receptor effect, the results suggest that the release of endogenous GRF is augmented following the cessation of electrical stimulation of neurons providing hypophysiotropic SS.
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PMID:Electrical stimulation of hypothalamic periventricular nucleus is followed by a large rebound secretion of growth hormone in unanesthetized rats. 204 88

The central action of peptides to influence GI motility in experimental animals is summarized in Table 1. TRH stimulates gastric, intestinal, and colonic contractility in rats and in several experimental species. A number of peptides including calcitonin, CGRP, neurotensin, NPY, and mu opioid peptides act centrally to induce a fasted MMC pattern of intestinal motility in fed animals while GRF and substance P shorten its duration. The dorsal vagal complex is site of action for TRH-, bombesin-, and somatostatin-induced stimulation of gastric contractility, and for CCK-, oxytocin- and substance P-induced decrease in gastric contractions or intraluminal pressure. The mechanisms through which TRH, bombesin, calcitonin, neurotensin, CCK, and oxytocin alter GI motility are vagally mediated. An involvement of central peptidergic neurons in the regulation of gut motility has recently been demonstrated in Aplysia, indicating that such regulatory mechanisms are important in the phylogenesis. Alterations of the pattern of GI motor activity are associated with functional changes in transit. TRH is so far the only centrally acting peptide stimulating simultaneously gastric, intestinal, and colonic transit in various animals species. Opioid peptides acting on mu receptor subtypes in the brain exert the opposite effect and inhibit concomitantly gastric, intestinal, and colonic transit. Bombesin and CRF were found to act centrally to inhibit gastric and intestinal transit and to stimulate colonic transit in the rat. The antitransit effect of calcitonin and CGRP is limited to the stomach and small intestine. The delay in GI transit is associated with reduced GI contractility for most of the peptides except central bombesin that increases GI motility. Nothing is known about brain sites through which these peptides act to alter gastric emptying and colonic transit. Regarding brain sites influencing intestinal transit, TRH-induced stimulation of intestinal transit in the rat is localized in the lateral and medial hypothalamus and medial septum. The periaqueductal gray matter is a responsive site for mu receptor agonist- and neurotensin-induced inhibition of intestinal transit. The neural pathways from the brain to the gut whereby these peptides express their stimulatory or inhibitory effects on GI transit is vagal dependent with the exception of calcitonin. It is not known whether the vagally mediated inhibition of GI transit by these peptides results from a decrease activity of vagal preganglionic fibers synapsing with excitatory myenteric neurons or an activation of vagal preganglionic neurons synapsing with inhibitory myenteric neurons. The lack of specific antagonists for these peptides has hampered the assessment of their physiological role.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system action of peptides to influence gastrointestinal motor function. 210 14

To determine the time onset of the growth hormone (GH) alteration in the genetically obese rat, we studied the in vivo and in vitro rat growth hormone releasing factor (rGRF(1-29)NH2)-induced GH secretion in 6- and 8-week-old lean and obese male Zucker rats. Under sodium pentobarbital anesthesia, rGRF(1-29)NH2 (GRF) was injected intravenously at two doses: 0.8 and 4.0 micrograms/kg b.w. Basal serum GH concentrations were similar in lean and obese age-matched animals. The GH response to both GRF doses tested was unchanged in 6-week-old obese rats as compared to their lean litter mates. In contrast, a significant decrease of the GH secretion in response to 4.0 micrograms/kg b.w. GRF was observed in the 8-week-old obese rats. The effect of GRF (1.56, 6.25 and 12.5 pM) was further studied in vitro, in a perifusion system of freshly dispersed anterior pituitary cells of lean and obese Zucker rats. Basal GH release was similar in the 6-week-old animal group. In contrast, it was significantly decreased in 8-week-old obese rats as compared to their lean litter mates. Stimulated GH response to 1.56 and 6.25 pM GRF was significantly greater in the 6-week-old obese group than in the age-matched control group. In contrast, the GH response to all GRF concentrations tested was significantly decreased in the 8-week-old obese rats as compared to their respective lean siblings. In 8-week-old obese rats, a decrease of GH pituitary content and an increase of hypothalamic somatostatin (SRIF) concentration were observed. Insulin and free fatty acid serum were significantly increased in 8-week-old obese rats. In contrast, lower insulin-like growth factor I serum levels were observed in the obese animals as compared to their lean litter mates. Finally, to further clarify the role of the periphery in the inhibition of GH secretion observed in the 8-week-old fatty rats, we exposed cultured pituitary cells of 8-week-old lean animals to 17% serum of their obese litter mates. A significant decrease of GRF-stimulated GH secretion of lean rat pituitary cells exposed to the obese serum was noted (P less than 0.05). This study demonstrates that, in the obese Zucker rat, an alteration of the GH response to GRF is evident by the 8th week of life. This defective GH secretion could be related to peripheral and central abnormalities.
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PMID:Dynamic of the GRF-induced GH response in genetically obese Zucker rats: influence of central and peripheral factors. 213 33

This study examines the effects of somatocrinin (GRF) and somatostatin antiserum (ASS) alone, and in combination, on liver growth. Twenty-four-day-old rats were injected s.c. twice daily for 14 days with either saline or GRF (4 and 20 micrograms X kg-1). ASS was given i.p. every 2 days. GRF alone had no effect on liver weight, but produced hyperplasia and increased RNA content. ASS alone had no effect on RNA, DNA, and protein contents. Potentiation of the effects of GRF by ASS was observed on liver weight and DNA content. Indeed, this combined treatment resulted in increased organ weight and hyperplasia at an intermediary level of GRF. These data indicate that a strong interaction exists between GRF and ASS on the control of liver growth, possibly through the release of growth hormone (GH).
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PMID:Effect of somatocrinin and a somatostatin antiserum on liver growth in the rat. 243 9

This study examines the effects of somatocrinin (GRF) and somatostatin antiserum (ASS), jointly and separately on gastric and duodenal growth. 24-day-old rats received twice daily SC injections of saline or GRF (4 and 20 micrograms X kg-1) for 14 days. ASS was given IP every 2 days. Alone, GRF increased gastric fundus weight concomitantly with DNA, RNA and protein contents producing hyperplasia and hypertrophy within this gland. Alone, ASS increased RNA and protein cellular concentrations. Joint ASS and GRF treatment stabilized the weight and protein content of the fundus, while reducing RNA contents as well as RNA and protein concentrations. GRF alone caused significant increments in duodenal weight and protein content suggesting cellular hypertrophy. Growth hormone, gastrin, cholecystokinin and secretin may be considered as putative mediators of these trophic effects.
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PMID:Effect of somatocrinin and a somatostatin antiserum on duodenal and gastric growth in the rat. 243 13

The current study examines the effects of somatocrinin (GRF) and somatostatin antiserum (ASS) alone and in combination on pancreatic growth. Twenty-four-day-old rats were injected daily s.c. at 10:00 and 16:30 h for 14 days with either saline or GRF (4 and 20 micrograms X kg-1). ASS was given i.p. every other day. Pancreatic weights and DNA, RNA, protein, amylase, and chymotrypsin total contents and concentrations were evaluated at the end of treatment. GRF alone was associated with significant decreases in pancreatic weight and contents of protein, amylase, and chymotrypsin but with significant increases in total DNA content indicating pancreatic atrophy and hyperplasia. ASS alone has a slight effect on DNA content but potentiates GRF given at the dose of 4 micrograms X kg-1. Even though ASS reduced protein and enzyme contents, it prevented the large decreases observed with increasing doses of GRF. These data present for the first time effects of GRF and ASS on pancreatic growth and describe a strong interaction between the two products. It is yet too early to determine how these two substances work on the pancreatic acinar cells, but hypotheses on their possible mode of action are proposed.
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PMID:Effect of somatocrinin with or without a somatostatin antiserum on pancreatic growth. 243 58

An increasing number of messengers have recently been found to coexist with growth hormone (GH)-releasing factor (GRF) in hypothalamic neurons. In view of a possible cosecretion of these substances with GRF into the portal circulation, the effect of synthetic rat hypothalamic GRF(1-43) alone, or together with dopamine (DA), L-dopa, gamma-aminobutyric acid (GABA), neurotensin (NT) or galanin (GAL) on GH release was investigated by using dispersed rat anterior pituitary cells in monolayer culture. GRF in concentrations of 10(-16)-10(-7) M stimulated GH release from somatotrophs in a dose-related manner. DA (10(-5) M), L-dopa (10(-8) and 10(-5) M) and GABA (10(-9) and 10(-5) M) did not affect basal GH release, whereas DA, but not L-dopa or GABA, significantly suppressed GRF-induced GH secretion. However, the inhibitory effect of DA on GRF-stimulated GH secretion was not observed in the presence of somatostatin (10(-6) M). NT (10(-6) M) and GAL (10(-6) M) did not change basal GH release. GAL, but not NT, inhibited GRF-stimulated GH release, but the addition of NT abolished the inhibitory actions of both GAL and DA. These results indicate that substances, probably coreleased with GRF from the same nerve endings, interact in the regulation of GH secretion at the pituitary level.
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PMID:Influence of coexisting hypothalamic messengers on growth hormone secretion from rat anterior pituitary cells in vitro. 244 97


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