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)

An in vitro dispersed hypothalamic cell system was developed and utilized to investigate the effect of exposure to cold stress prior to sacrifice on release of somatostatin-like immunoreactivity (SRIF-LI). Exposure of the rats to cold stress prior to sacrifice significantly increased basal (or control) release of SRIF-LI from dispersed hypothalamic cells. The endogenous opiate peptides (beta-endorphin, Met-enkephalin and Leu-enkephalin)significantly inhibited the basal release of SRIF-LI from dispersed hypothalamic cells obtained from rats exposed to the cold prior to sacrifice. Naloxone, a specific opiate antagonist, had no effect on basal release but blocked inhibition by the endogenous opiate peptides. In marked contrast, the endogenous opiate peptides had no effect on basal release of SRIF-LI from dispersed hypothalamic cells of rats exposed to room temperature prior to sacrifice.
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PMID:Opiate peptides modulate somatostatin release from dispersed hypothalamic cells. 612 May 3

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
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PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11

Administration of somatostatin intracerebroventricularly to mice produced a dose-dependent mydriasis, whereas intravenous injections were ineffective. Naloxone could prevent or abolish this effect. It is suggested that somatostatin either directly excites opiate receptors or activates endopioid pathways involved in the regulation of pupillary size.
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PMID:Somatostatin mydriasis in mice. 613 66

A role for the enkephalins in the regulation of gastric somatostatin (SLI) secretion has been investigated in an isolated perfused rat stomach model. Both methionine- and leucine-enkephalins caused a dose-dependent inhibition of gastric inhibitory polypeptide (GIP) stimulated SLI secretion. Leu-enkephalin was one order of magnitude less potent than met-enkephalin: 50% inhibition by met-enkephalin was at 4 X 10(-9) M and with leu-enkephalin 3.5 X 10(-8) M. Naloxone (100 nM) had no effect on basal secretion but blocked the inhibitory action of met-enkephalin (1 nM or 1 microM). Vagal stimulation (7 V, 10 Hz, 5 ms) inhibited GIP-stimulated SLI release. Administration of naloxone partially reversed this inhibition, suggesting that endogenous opioids were at least partially responsible for vagally induced inhibition. A number of possible pathways by which endogenous enkephalins may modulate SLI release have been proposed.
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PMID:Enkephalinergic control of somatostatin secretion from the perfused rat stomach. 613 72

Previously, we have demonstrated the effects of exogenously administered opiates on somatostatin release in dogs and therefore the present study was designed to determine the effect of endogenous opiates via naloxone-induced opiate receptor blockade on somatostatin release. Additionally, plasma insulin and pancreatic polypeptide (PP) levels were determined in response to intragastrically instilled protein, carbohydrate and fat test meals in a group of eight conscious dogs. To all test meals either naloxone (4 mg) or saline was added. The rise of plasma somatostatin levels in response to liver extract, sucrose and fat was attenuated significantly by naloxone. Naloxone had no effect on the rise of postprandial plasma insulin and PP levels. The present data demonstrate that endogenous opiates have a stimulatory effect on postprandial somatostatin release in dogs which indicates a tight interaction that might be of relevance for nutrient homeostasis.
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PMID:Evidence for a role of endogenous opiates in postprandial somatostatin release. 613 19

Modulation of feeding by opiates, putative satiety peptides, and dopamine was explored in the Chinese hamster, an animal that develops diabetes mellitus in certain inbred strains. Diabetic hamsters were hyperphagic relative to their nondiabetic controls, but both groups exhibited natural circadian variation in feeding. Starvation provoked hyperphagia of about 1-h duration in both groups. Naloxone and butorphanol had no effects on Chinese hamster feeding. Opiate receptor binding on Chinese hamster brains demonstrated no specific binding of naloxone or ethylketocyclazocine, but IR-dynorphin concentrations were comparable with that in rats. N-allylnormetazocine, a sigma-opiate receptor agonist, appeared to stimulate diabetic hamster feeding. Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. Calcitonin limited feeding in both groups but may be nonspecific. Dopaminergic blockade by haloperidol also limited feeding, and diabetic hamsters were more sensitive to this. Although Chinese hamsters clearly can modulate their food intake when diabetic, we conclude that the opiatergic and peptidergic influences on feeding are very different from those in rats and may be of little importance.
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PMID:Feeding systems in Chinese hamsters. 614 21

Although the incidence of obesity in the domesticated dog is high, few studies have investigated the regulation of food intake in this species. In the present study we investigated the response of the dog to a number of putative satiety agents including cholecystokinin (CCK), bombesin, calcitonin and naloxone. CCK significantly suppressed food intake during a scheduled fifteen minute meal in intact dogs and in dogs receiving total subdiaphragmatic vagotomies. Emesis occurred following injection of higher doses of CCK in most dogs. Bombesin and calcitonin reduced intake in both normal and vagotomized dogs, although higher doses of calcitonin were needed to significantly suppress feeding in vagotomized dogs compared with intact animals. Naloxone reduced feeding by as much as 60% in intact and vagotomized animals. Glucagon suppressed feeding in intact dogs, but not in vagotomized animals. Somatostatin and pancreatic polypeptide did not alter food intake. Thus the domesticated dog responds somewhat differently to some neuropeptides compared with the laboratory rat stressing the importance of examining the regulation of food intake across species.
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PMID:Peptidergic regulation of feeding in the dog (Canis familiaris). 614 23

In pentobarbital-anesthetized rabbits, iv injection of 9 nmol (31 micrograms) human beta-endorphin (beta h-endorphin)/kg BW caused a significant (P less than 0.05) increase in serum glucose and a significant decline in serum insulin during the subsequent 60 min. When 9 nmol/kg BW beta h-endorphin were injected simultaneously with 0.7 g glucose/kg BW, the clearance of serum glucose and the expected glucose-stimulated rise in serum insulin were both inhibited. The threshold dose for the insulinopenic effect of beta h-endorphin in the anesthetized, glucose-loaded rabbit was 0.09 nmol/kg BW. Threshold doses/kg BW were determined for six structurally related peptides found to possess insulinopenic activity: camel beta-endorphin, 0.09 nmol; N-arg-beta h-endorphin, 0.09 nmol; D-ala2-beta h-endorphin, 0.09 nmol; leu5-beta h-endorphin, 0.09 nmol; met-(O)5-beta h-endorphin, 0.9 nmol; and beta h-endorphin1-27, 0.9 nmol. Threshold dose/kg BW for somatostatin was 9 nmol. The following compounds were inactive at 9 nmol/kg BW: N-acetyl-beta h-endorphin; N-acetyl-arg-beta h-endorphin; beta h-endorphin2-31; beta h-endorphin6-31; beta h-endorphin(((1-5 + 6-31))); beta h-endorphin1-18 (gamma-endorphin); beta h-endorphin1-17 (alpha-endorphin); beta h-endorphin1-5 (met-enkephalin); leu5-beta h-endorphin (leu-enkephalin); met-NH2(5)-beta h-endorphin1-5 (met-enkephalinamide); D-ala2-leu5-beta h-endorphin1-5; D-ala2-N-me-phe4, met-(O)5-ol-beta h-endorphin1-5; and D-ala2-D-leu5-beta h-endorphin1-5. Ninety nmoles per kg BW of naloxone did not alter the insulinopenic effect of 0.9 nmol/kg BW beta h-endorphin. As little as 2.9 X 10(-10) molar beta h-endorphin inhibited glucose-stimulated release of insulin by rabbit pancreas slices in vitro. The capacities of the peptides and alkaloids to inhibit insulin secretion in vitro followed the same general order as the in vivo insulinopenic capacities. Naloxone at 2.9 X 10(-6) M did not reduce the antisecretagogue effect of 2.9 X 10(-8) M beta h-endorphin. These findings, when compared with previously described structure-activity relationships for opioid receptors, indicate the presence of a novel receptor for beta-endorphin in rabbit pancreas, the activation of which inhibits glucose-stimulated secretion of insulin.
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PMID:Effects of opioid peptides and opiate alkaloids on insulin secretion in the rabbit. 633 12

The role of endogenous opioid peptides in mediating the endocrine and metabolic response to pelvic surgery was investigated. Fourteen patients were studied; seven were infused with the specific opioid antagonist, naloxone, at a rate of 20 micrograms kg-1 (body weight) hr-1, while the remainder acted as a control group. Naloxone exacerbated the glycaemic response to surgery but had no statistically significant effect on changes in the glycoregulatory hormones, pancreatic glucagon, insulin, cortisol and growth hormone. However, there was a wide individual variation in the glucagon response to naloxone with marked stimulation in some patients. Naloxone infusion increased plasma pancreatic polypeptide secretion during the 1st hour of surgery and reversed the decline in plasma motilin concentrations, but had no effect on circulating somatostatin, vasoactive intestinal polypeptide, gastrin, enteroglucagon and neurotensin values. We conclude that endogenous opioid peptides have only a limited role in modulating the endocrine and metabolic response to surgery.
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PMID:The effects of naloxone on circulating metabolites, glycoregulatory hormones and gut peptides during pelvic surgery. 668 26

The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombesin-like immunoreactivity (BLI), somatostatin and gastrin from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer. Vagal stimulation was performed for 10 min with 1 ms, 10 V and 2, 5, 10 or 20 Hz, respectively. In control experiments BLI release increased significantly above basal secretion during a stimulation frequency of 10 Hz (1367 +/- 357 pg/10 min; P < 0.001) and 20 Hz (996 +/- 202 pg/10 min; P < 0.01), but not at 2 and 5 Hz. In comparison to the controls naloxone (10(-6) M) significantly increased BLI secretion at 5 Hz by 573 +/- 150 pg/10 min (P < 0.05), but attenuated the BLI response to higher stimulation frequencies of 10 and 20 Hz to 284 +/- 143 pg/10 min (P < 0.001) and 490 +/- 114 pg/10 min (P < 0.01), respectively. At 2 Hz naloxone had no effect on BLI release. As shown previously the cholinergic blocker atropine (10(-7) M) induced a significant BLI release during vagal stimulation at 2 Hz (680 +/- 233 pg/10 min; P < 0.01) and 5 Hz (935 +/- 324 pg/10 min; P < 0.05), but was without effect at 10 and 20 Hz compared to the controls. The effects of the combination of naloxone and atropine were similar to naloxone and atropine alone. Naloxone had no effect on vagal or GRP-induced regulation of gastrin and somatostatin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of endogenous opioids on vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from the perfused rat stomach. 775 6


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