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)

Chronic hyperglycemia in diabetes is a major causative factor of free radical generation which further leads to many secondary diabetic complications via the damage to cellular proteins, membrane lipids, and nucleic acids. Zinc is an essential trace element in all living systems and plays a structural role in many proteins and enzymes. Somatostatin is known to have inhibitory effects on various gastrointestinal functions. Therefore, we determined somatostatin protein production and secretion levels, and biochemical and light microscopical changes following zinc supplementation in the gastrointestinal tract of streptozotocin (STZ)-diabetic rats. The animals were divided into four groups: Group I: control (untreated) animals; Group II: control animals given zinc sulfate; Group III: diabetic animals; and Group IV: diabetic animals given zinc sulfate. Zinc sulfate was given to the animals by gavage at a daily dose of 100 mg/kg body weight for 60 days. Diabetes was induced by intraperitoneal (i.p.) injection of STZ in a single dose of 65 mg/kg. For histological studies, stomach and duodenum tissues were fixed in Bouin solution and sections stained with Masson's trichrome and Periodic-Acid-Schiff. Tissue homogenates were used for protein, lipid peroxidation (LPO), glutathione (GSH), and nonenzymatic glycosylation (NEG) analyses. Zinc supplementation to the STZ-diabetic rats revealed the protective effect of zinc on these parameters. Zinc supplementation may contribute to prevent at least some complications of diabetes mellitus.
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PMID:Alterations in somatostatin cells and biochemical parameters following zinc supplementation in gastrointestinal tissue of streptozotocin-induced diabetic rats. 1746 Jul 67

The aim of this study was to investigate the effects of zinc supplementation on somatostatin and insulin peptide expressions and biochemical parameters. Six- to 6.5-month-old female Swiss albino rats weighing 150-200 g were used. The animals were divided into four groups: group I: control (intact) animals; group II: control animals given zinc sulfate; group III: streptozotocin (STZ)- induced diabetic animals; group IV: STZ-induced diabetic animals given zinc sulfate. Fasting blood glucose and glutathione levels were measured at 0, 1, 30 and 60 days. On day 60, the pancreas tissue and blood samples were taken from the animals. Zinc supplementation caused a decrease in hyperglycemia, as well as weight increase. Zinc sulfate treatment did not affect the number of somatostatin-immunoreactive cells in the pancreas. More insulin-immunoreactive cells were observed in the pancreatic islets of the diabetic+zinc sulfate group than in the diabetic group, although it was not statistically significant. The results show that zinc supplementation may prevent diabetes in experimental animals.
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PMID:The influence of zinc supplementation on the pancreas of streptozotocin-diabetic rats. 1911 23