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)

In a previous study it was shown that Raynaud patients during ischemic attacks displayed significantly lower levels of vasoactive intestinal polypeptides (VIP) in cubital vein plasma than did normal subjects in the same relatively cold environments. Low-frequency transcutaneous nerve stimulation (TNS), producing widespread cutaneous vasodilatation, was associated with a 30-35% increase in plasma VIP in both groups. In the present study parallel observations were made in some of the same subjects under the same experimental conditions with regard to six other gastrointestinal peptides: somatostatin, motilin, pancreatic polypeptide (PP), secretin, gastric inhibitory polypeptide (GIP), and cholecystokinin (CCK), determined radioimmunochemically. Except for CCK, the mean plasma levels of all these gut peptides were similarly lower in the Raynaud patients than in the normal subjects in cold environments. However, TNS did not induce significant increases in the plasma levels of any of these 6 peptides. These findings appear to place VIP in a different functional category than the other gut peptides.
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PMID:Lower plasma levels of some gastrointestinal peptides in Raynaud's disease. Influence of transcutaneous nerve stimulation. 387 78

Centrally administered neuropeptides were investigated for their effects on the development of gastric lesions in rats. Thyrotropin releasing hormone (TRH), vasoactive intestinal peptide (VIP) and gonadotropin releasing hormone (LHRH) produced gastric lesions acutely, with TRH demonstrating the most pronounced effect in terms of incidence and severity. Ten-fold higher doses of the same peptides administered intravenously produced none or very few gastric lesions. Moreover, pretreatment with atropine partially inhibited their production. Corticotropin releasing factor (CRF) exhibited only mild ulcerogenic effects, and the gastric lesions induced with this peptide developed more slowly than with TRH, VIP and LHRH. Although ulcerogenic in their own right, none of these four neuropeptides significantly potentiated the potent ulcerogenic effects of cold-restraint stress. Since other neuropeptides, including somatostatin, human pancreatic growth hormone releasing factor (hpGRF), substance P, bombesin, and neurotensin, had no demonstrable effects on gastric mucosa, we can conclude that the lesions were not a general effect of intracisternal administration of neuropeptides. The results suggest that within the central nervous system, there are several neuropeptides that play a significant role in the development of gastric lesions via, at least in part, vagal-dependent mechanisms.
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PMID:The effects of centrally administered neuropeptides on the development of gastric lesions in the rat. 392 Apr 62

A soluble somatostatin binding factor was detected in cell-free extracts from chicken pancreas. For binding measurements Tyr1-somatostatin was radio-labeled with 125I by the lactoperoxidase technique. Specific radioactivity of about 18.5 MBq/nmol was achieved. Maximal total binding is approximately 0.17 (B/T) in the presence of 30 mg/l pancreatic protein. The specific binding is 0.10 and is suppressed by addition of 1 mg/l synthetic cold cyclic somatostatin. The dose-response curve of synthetic cyclic somatostatin is in the range of 0.6-600 nmol/l. Ca2+ and reduced thiol-reagents inhibit the specific binding. Insulin, glucagon and corticotropin show a low, and luliberin and reduced somatostatin a high cross-reactivity. Molecular weight was estimated by gel filtration and the specific binding molecule was eluted at a Kav = 0.2 on an Ultrogel (AcA 54) column. This corresponds to Mr 40 000. Electrophoretic properties of the binding complex and semipurification by polyacrylamide disc gel electrophoresis: relative mobility of the 125I-Tyr-somatostatin binding complex is about 0.6. Relative mobilities of binding-protein fractions are 0.71 and 0.74. Highest relative specific binding was detected in the (100 000 g) cytosol fractions. Binding with cell-free extracts from the splenic lobe area was 4-fold higher than that from other parts of the chicken pancreas.
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PMID:Somatostatin binding factor from chicken pancreas. 611 81

The role of the endocrine pancreas in glucose production (Ra), utilization (Rd), and metabolic clearance (R'd) was investigated during acute exposure to cold in normal normothermic dogs. Two ambient temperatures (TaN = +25 degrees C and TaC = -21 degrees C) were selected. At TaC, metabolic rate and glucose turnover of the shivering dogs were 4.3 and 2.4 times, respectively, higher than in dogs resting at TaN. As compared with the pre-experimental period, somatostatin infusion at TaN induced a 25% (arterial) and 34% (portal) glucagon deficiency, while insulin concentration dropped by 59% (arterial) and 74% (portal). Similar values were obtained at TaC for glucagon (39% arterial and 47% portal) and for insulin (52% arterial and 56% portal). At TaN, these simultaneous hormonal alterations provoked a slight reduction in plasma glucose concentration which levelled down to 4.4 mM. This reduction was due to a decrease in Ra, followed by a parallel decrease in Rd whereas R'd remained unchanged. At TaC, plasma glucose concentration dropped to the same level but quickly rose again during somatostatin infusion. This rise was due to a larger reduction in Rd than in Ra, accompanied by an abrupt fall in R'd. This reduction in R'd appears to be an important mechanism able to restore euglycemia during global pancreatic hormone deficiency in cold exposed dogs.
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PMID:Combined effects of cold and somatostatin on glucose kinetics in dogs. 611 59

In dogs, selective insulin deficiency induced by simultaneous somatostatin and glucagon infusion does not alter the high rate of glucose utilization provoked by acute cold exposure. However, both in resting and in shivering dogs, lowering of plasma insulin decreases plasma glucose metabolic clearance significantly.
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PMID:Independence of circulating insulin levels of the increased glucose turnover in shivering dogs. 611 62

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

Neurotensin, a peptide common to brain and gastrointestinal tissue, has been reported common to brain and gastrointestinal tissue, has been reported to inhibit both gastric acid secretion and gastric mucosal blood flow after central nervous system administration in rats. Therefore, the effect of intracisternal neurotensin on the development of gastric ulcers induced by cold-plus-restraint stress in the rat was studied. Following intracisternal injection, neurotensin (20-30 micrograms) significantly inhibited the development of gastric ulcers in this model. This effect was shown to be both dose related and route specific, inasmuch as neither lower doses of intracisternal neurotensin nor intravenous neurotensin were cytoprotective. In addition, potential actions of central neurotensin that may have mediated this beneficial effect were tested by administering somatostatin or oxotremorine intracisternally and cimetidine or haloperidol intraperitoneally. In contrast to intracisternal neurotensin, none of these substances reduced the incidence of gastric ulcers in this model. This was true despite the fact that cimetidine, but not neurotensin, significantly increased gastric pH. Finally, when cold-plus-restraint-stressed rats were pretreated with indomethacin, an inhibitor of prostaglandin synthesis, the cytoprotective effect of neurotensin was completely abolished. These results suggest that intracisternal neurotensin exerts a significant cytoprotective effect for stress-induced gastric ulcers in rats. This effect, which is mediated by the central nervous system, does not appear to be related to changes in body temperature, neuroleptic-like properties, or gastric acid secretion but requires an intact prostaglandin synthetic pathway.
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PMID:Cytoprotective effect of centrally administered neurotensin on stress-induced gastric ulcers. 612 89

Bombesin and the somatostatin analog, desAA-[D-Trp8]-somatostatin (ODT8-SS), act within the central nervous system to alter animals' oxygen consumption (VO2) in a manner consistent with the observed effects of these peptides on temperature regulation. Bombesin given intracerebroventricularly (i.c.v.) to rats at cold ambient temperatures prevents elevation of VO2 but does not lower VO2 below the values observed at thermoneutrality. ODT8-SS given i.c.v. increases VO2 of animals at an ambient temperature of 20 degrees C and prevents bombesin inhibition of VO2 at low ambient temperatures. Thus, bombesin inhibits VO2 induced by cold and results in hypothermia, ODT8-SS prevents bombesin-induced inhibition of VO2 and bombesin-induced hypothermia and, ODT8-SS increases VO2 and produces hyperthermia in animals at thermoneutral temperatures.
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PMID:Bombesin and somatostatin related peptides: effects on oxygen consumption. 612 48

An intracisternal injection of somatostatin-28 produced hyperthermia in rats at cold, thermoneutral, warm ambient temperatures. The hyperthermic response to somatostatin-28 was not prevented by pretreatment of rats with the following agents: alpha-methylparatyrosine, phenoxybenzamine, propranolol, sulpiride, atropine, methysergide or naloxone. Somatostatin-28 prevented hypothermia induced by bombesin and gamma-MSH when it was administered simultaneously, but it left the hyperthermic response to TRH intact. The results indicate that somatostatin-28 produces hyperthermia by elevating a "set point" or regulated level of temperature. Under the conditions tested, the hyperthermic response to somatostatin-28 does not appear to be dependent on muscarinic cholinergic, serotonergic, alpha- or beta-adrenergic, dopaminergic or endogenous opiate system.
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PMID:Hyperthermic action of somatostatin-28. 613 57

The studies described in this paper support the hypothesis that specific brain peptides may act as neurochemical substrates for the differential patterns of sympathetic nervous system and adrenomedullary responses to various provocative stimuli. Different treatments, e.g., exposure to ether vapor or cold, hemorrhage or hypoglycemia, elicit stimulus-specific changes in plasma concentrations of epinephrine and norepinephrine. Likewise, several neuropeptides, e.g., bombesin, corticotropin-releasing factor, thyrotropin-releasing factor, and somatostatin-related peptides, act within the central nervous system to produce differential changes in the relative concentrations of epinephrine and norepinephrine in plasma. The possibility that these peptides may be involved in generating stimulus-specific changes in plasma catecholamine concentrations following various physiological and pharmacological treatments is discussed.
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PMID:Brain peptide regulation of adrenal epinephrine secretion. 614 62


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