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)

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

The relative contribution of hyperglucagonemia to the mechanisms of nitrogen loss during catabolic states has not been clearly established. The present study examines the independent effect of physiologic elevations of plasma glucagon on whole-body protein kinetics, as well as on net amino acid balance across the liver and gastrointestinal tract tissues, in conscious 18-hour-fasted dogs (n = 7). Each study consisted of a 120-minute equilibration period, a 30-minute basal period, and a 150-minute experimental period. Leucine kinetics were measured using L-[1-14C]leucine. Pancreatic hormones were maintained by infusing intravenous somatostatin (0.8 micrograms/kg.min), intraportal insulin (275 microU/kg.min), and intraportal glucagon (0.65 ng/kg.min basally and 2.5 experimentally). Dextrose was infused to maintain plasma glucose constant (14.1 +/- 0.3 mumol/L), thereby providing a consistent metabolic steady state for the study of protein and amino acid metabolism. In the experimental period, plasma glucagon was fourfold basal levels (112 +/- 10 v 32 +/- 6 pg/mL), whereas plasma insulin remained stable (mean, 10 +/- 1 microU/mL). Hepatic glucose production was increased 30%, but leucine rates of appearance ([Ra] proteolysis), oxidative disappearance (Rd), and nonoxidative Rd (protein synthesis) were not altered during the experimental period. Furthermore, the net release of amino acids by the gastrointestinal tract was not increased by glucagon. However, uptake and extraction of amino acids by the liver were increased, resulting in a 17% decrease in total plasma amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of glucagon in the control of protein and amino acid metabolism in vivo. 799 Jul 4

Emergency therapy of sulfonylurea overdoses with glucose is often unsatisfactory because glucose stimulates insulin release and initiates a need for escalating quantities of hypertonic glucose to maintain normoglycemia. We tested the hypothesis that octreotide, an analog of somatostatin, would reverse hyperinsulinemia induced by a sulfonylurea overdose. Eight normal subjects received glipizide (1.45 mg/kg) on three occasions. Within 3 h, all subjects became hypoglycemic (< 50 mg/dL) and were initially treated with 50% dextrose followed by 1) dextrose infusion, 2) octreotide (30 ng/kg.min, iv), or 3) diazoxide (300 mg, iv, every 4 h). Euglycemia (85 mg/dL) was maintained with supplementary dextrose in treatment limbs 2 and 3. Insulin concentrations were 4-5 times greater with dextrose alone or in combination with diazoxide than with octreotide (P < 0.01). Dextrose requirements during diazoxide or dextrose alone were not different, but were both greater than those during octreotide treatment (P < 0.0001). All therapies were stopped at 13 h. Glucose levels remained above 3.6 mmol/L (65 mg/dL) in six of eight subjects receiving octreotide for the remaining 4 h. Glucose fell to below 3.6 mmol/L within 1.5 h of stopping either dextrose or diazoxide in each subject. Overall, octreotide reduced and in four of eight subjects entirely eliminated the need for exogenous glucose after a large overdose of glipizide. We conclude that octreotide is safe and effective and should be strongly considered as a logical therapeutic alternative for this metabolic emergency.
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PMID:Octreotide reverses hyperinsulinemia and prevents hypoglycemia induced by sulfonylurea overdoses. 844 35