125 36 36 3 3 M. C. Cam R. A. Pederson R. W. Brownsey J. H. McNeill Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences University of British Columbia Vancouver Canada MRC Regulatory Peptide Group, Department of Physiology University of British Columbia Vancouver Canada Department of Biochemistry, Faculty of Medicine University of British Columbia Vancouver British Columbia Canada Summary Recent studies have demonstrated the insulin-like effects of oral vanadyl sulphate in the streptozotocin-diabetic rat, including the amelioration of hyperglycaemia and the prevention of diabetes-related cardiac and adipose tissue dysfunction. However, the possibility that vanadyl treatment, routinely initiated at 3 days after the induction of diabetes, had prevented the full cytotoxic destruction of the beta cell, and thus accounted for the apparent anti-diabetic properties of vanadyl was questioned. Hence in the present study, we examined the effectiveness of vanadyl sulphate as a glucose-lowering and anti-diabetic agent when administration was delayed from the time of induction of diabetes. Male Wistar rats were injected with a single intravenous dose of streptozotocin (55 mg/kg). Vanadyl sulphate was administered in the drinking water at a concentration of 0.75 mg/ml from 3, 10 and 17 days after the streptozotocin injection and treatment was then maintained for 5 months. Vanadyl intake was accompanied by lowered serum levels of triglyceride and cholesterol with no associated enhancement in circulating insulin. Vanadyl-treated diabetic animals showed improved glucose tolerance while insulin release in vivo was still markedly lower than in non-diabetic rats. Adipose tissue function, as expressed by basal and epinephrine-stimulated lipolysis in isolated adipose tissue, was also normalized in vanadyl-treated diabetic animals. These responses were all observed whether vanadyl treatment was initiated 3, 10 or 17 days after induction of diabetes. Finally, prolonged treatment with vanadyl sulphate (in this case up to 5 months) did not cause any apparent hepatic toxicity as assessed histologically. Diabetes-induced morphological changes in the kidney were also prevented by vanadyl treatment. Thus, these findings support the concept that the efficacy of vanadyl treatment is unrelated to protection from the acute toxic effects of streptozotocin on pancreatic beta cells. Further, these studies provide additional support for the notion suggested in earlier studies that either improved pancreatic function may result from the alleviation of hyperglycaemia by vanadium treatment or that some residual pancreatic function which in itself is insufficient to prevent the onset and progression of the diabetic state may contribute to an effective response to administered vanadium.
Diabetologia – Springer Journals
Published: Mar 1, 1993
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