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 vitro degradation of 125I-labeled somatostatin-14 (Tyr11) [I-SS-14(Tyr11)] by luminal flushings of rat gastrointestinal segments was studied to characterize the fate of somatostatin in the gastrointestinal lumen. In addition, we evaluated the effect of rat milk as a potential inhibitor of luminal degradation of 125I-SS-14(Tyr11). Degradation of 125I-SS-14(Tyr11) was not detected in stomach flushings from either suckling or weanling rats. Luminal flushings from the small intestine degraded 125I-SS-14(Tyr11), with a gradient increase of activity from duodenum to midjejunum (degradation in suckling rat midjejunum and ileum was about five times lower than that in weanling rat). Degradation of 125I-SS-14(Tyr11) by luminal flushings of suckling rat midjejunum was dose dependently inhibited by rat milk casein and soluble fractions. Inhibitory activity of rat milk soluble fraction was heat labile and several times more potent than that of casein fraction. Casein fraction appeared to be stable at 100 degrees C for up to 30 min of exposure. These studies suggest that somatostatin is stable in the gastric lumen and that milk protects somatostatin from intestinal luminal proteolysis, indicating a possible physiological significance of milk-borne SS-14 for the suckling rat gastrointestinal tract.
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PMID:Inhibition of intestinal degradation of somatostatin by rat milk. 196 33

Regulation of cholecystokinin (CCK) secretion was studied in conscious unrestrained rats by simultaneous duodenal perfusion with foodstuffs, intravenous infusion of hormones or neural agents, and arterial blood sampling for CCK bioassay. Duodenal infusion of casein resulted in elevation of plasma CCK from fasting level of 0.5 +/- 0.1 to 3.8 +/- 0.4 pM. Casein hydrolysate, calcium, and glucose did not elevate plasma CCK. Infusion of intact fat had a small, but nonsignificant, effect (1.4 +/- 0.4 pM), whereas infusion of oleate increased plasma CCK to 3.7 +/- 0.6 pM. Thus intact protein and fatty acids are the major dietary intestinal stimuli for CCK release in the rat. The CCK response to protein could be inhibited by somatostatin but not by peptide YY (0.2, 2, or 20 micrograms.kg-1.h-1); intravenous infusion of 1 or 10 micrograms.kg-1.h-1 somatostatin decreased casein-stimulated CCK levels to 1.5 +/- 0.2 and 0.9 +/- 0.3 pM, respectively. Stimulation of vagal discharge with 2-deoxy-D-glucose had no effect on basal or protein-stimulated plasma CCK levels; thus CCK release in the rat does not appear to be modulated by central vagal pathways. Gastrin-releasing peptide increased fasting plasma CCK levels to 1.6 +/- 0.1 pM. Administration of the cholinergic agonist bethanechol, while having no effect on fasting CCK level, inhibited protein-stimulated plasma CCK from 3.9 +/- 0.6 to 1.3 +/- 0.3 pM. Cholinergic blockade with atropine, in contrast, had no effect on basal or protein-stimulated plasma CCK. Thus CCK release is stimulated by dietary protein or fatty acid and by gastrin-releasing peptide and inhibited by somatostatin and bethanechol.
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PMID:Regulation of cholecystokinin secretion by food, hormones, and neural pathways in the rat. 197 Jul 7

Specific radioimmunoassay were used to measure somatostatin and vasoactive peptide in portal and peripheral plasma from conscious dogs prepared with indwelling portal catheters. In six animals with intact stomachs, a test meal induced a significant rise of portal and peripheral somatostatin, while the significant response of vasoactive intestinal peptide in portal plasma was not reflected in peripheral blood. Similar somatostatin and vasoactive intestinal peptide responses were observed in six dogs previously submitted to antrectomy and Billroth I anastomosis, when given the same test meal, while the gastrin response was 20% of the response in the intact dogs (P < 0.01). The effects of intragastric instillation of 300 ml dextrose, casein hydrolysate, and Intralipid, adjusted to 300 mosmol/kg and pH 7.0, were studied in six dogs with intact stomachs. Casein and Intralipid induced significant increases of somatostatin in portal and peripheral plasma, while VIP increased after Intralipid only, both in portal and peripheral blood. Dextrose resulted in no significant variation of either peptide in portal or in systemic plasma. Intraduodenal infusion of isotonic bile induced a significant release of somatostatin, both in portal and peripheral plasma, but no significant vasoactive intestinal peptide response. These results indicate that several factors can evoke a significant release of somatostatin in dogs, and that the variations of the peptide concentration in portal plasma are reflected in peripheral blood. Among the factors tested, only intragastric fat evoked a vasoactive intestinal peptide response that could be measured in peripheral blood.
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PMID:Effects of test meal, intragastric nutrients, and intraduodenal bile on plasma concentrations of immunoreactive somatostatin and vasoactive intestinal peptide in dogs. 610 20