Treatment of diabetes with vanadium salts: general overview and amelioration of nutritionally induced diabetes in the Psammomys obesus gerbil.

摘要: Background Numerous investigations have demonstrated the beneficial effect of vanadium salts on diabetes in streptozotocin (STZ)-diabetic rats, rodents with genetically determined and human subjects. The amelioration included abolition hyperglycemia, preservation insulin secretion, reduction hepatic glucose production, enhanced glycolysis lipogenesis improved muscle uptake through GLUT4 elevation translocation. molecular basis salt action is not yet fully elucidated. Although evidence has been provided that receptor activated, possibility exists cytosolic non-receptor tyrosine kinase, direct phosphorylation IRS-1 activation PI3-K, leading to translocation, are involved. raised proteins signaling pathway appears be related inhibition protein phosphatase (PTPase) activity by salts. Novel experiments The model utilized our study was Psammomys obesus (sand rat), a desert gerbil which becomes hyperglycemic hyperinsulinemic an ad libitum high energy (HE) diet. In contrast previously investigated deficient models, vanadyl sulphate used correct resistance hyperinsulinemia, led β-cell loss. Administration 5 mg/kg sulfate for 5 days resulted prolonged restoration normoglycemia normoinsulinemia most animals, return tolerance normal, phosphoenolpyruvate carboxykinase activity. There no change food consumption regular growth during or after treatment. Pretreatment sulfate, followed transfer HE diet, significantly delayed onset hyperglycemia. Hyperinsulinemic-euglycemic clamp treated improvement utilization. However, ineffective when administered animals lost their secretion capacity protracted but substantially reduced hyperglycemia given together exogenous insulin. vitro liver receptors isolated from ineffective. vivo treatment restored total mRNA contents addition membrane protein, accordance increased utilization study. These results indicate short-term corrects nutritionally induced, resistant diabetes. This requires presence its effect. Thus, P. result potentiation rather than mimicking, probably distal receptor. Copyright © 2000 John Wiley & Sons, Ltd.