ISSN No. 1606-7754                   Vol.14 No.3  December 2006

Low doses of vanadyl sulfate protect rats from lipid peroxidation and hypertriglyceridemic effects of fructose-enriched diet
Mehdi Harati1, Mohsen Ani2
Department of Biochemistry, Faculty of Medicine, Zahedan University of Medical Sciences, Zahedan1 Department of Biochemistry, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran2

Abstract

Background: Insulin resistance, hyperinsulinemia and disturbances in lipid metabolism can be produced in healthy rats by feeding them a fructose-enriched diet. Vanadyl sulfate, an antidiabetic trace element, enhances insulin sensitivity in type 2 diabetic patients. The aim of this study was to determine the effect of vanadyl sulfate treatment (0.2 mg/ml in drinking water for 7 days) on plasma insulin, triglyceride concentration and plasma lipid peroxidation in rats that were fed a fructose-enriched diet that leads to insulin resistance. Methods: Male Wistar rats were divided into four groups: fructose-fed rats (FF); vanadyl sulfate treated-fructose fed treated rats (FV); control rats (C); and vanadyl sulfate-treated control rats (CV). Control and vanadyl sulfate-treated control rats were fed with standard laboratory chow. Results: High fructose feeding resulted in hyperinsulinemia and hypertriglyceridemia, and the plasma lipid peroxidation marker TBARS (thiobarbituric acid reactive substances) was significantly elevated. Administration of vanadyl sulfate was associated with significant normalization of plasma insulin and triglyceride levels. These rats also showed significantly lower TBARS than untreated, fructose-fed rats. Conclusion: We conclude that enhanced lipid peroxidation occurs in addition to hypertriglyceridemia in fructose-fed rats. It is suggested that lipid peroxidation associated with hypertriglyceridemia may be responsible for the pathologies induced by high fructose consumption. The plasma insulin level probably contributes to this increased peroxidation. Improved insulin action in fructose-fed vanadyl sulfate treated rats could be responsible for the amelioration of those abnormalities induced by fructose feeding. (Int J Diabetes Metab 14: 134-137, 2006)

Keywords: Insulin resistance, Vanadyl sulfate, TBARS, Triglyceride, Fructose.

Introduction

It has recently been shown that rats fed a fructose-enriched diet, that induces insulin resistance, develop oxidative stress. This oxidative stress improved when the diet was supplemented with antidiabetic agents.1 An increasing number of studies have focused on the role of antidiabetic agents on lipid peroxidation.2 Vanadium, an ultratrace element, is a new antidiabetic element,3 that is used in experimental studies for the management of diabetes mellitus.4 Because vanadium salts are used in glycemic homeostasis, their effects may depend strongly on changing insulin sensitivity in the liver and probably at the level of skeletal muscle.5 The mechanisms of action of vanadium are not yet fully understood. The improvement in glucose uptake by the peripheral tissues could result from increased insulin binding to its membrane receptors, from the activation of post receptor metabolic pathways, as well as from a beneficial effect on lipid metabolism.6 Although it was shown that vanadium compounds may increase lipid peroxidation,7 it is unknown whether low doses of vanadyl ion (as vanadyl sulfate) in short term treatments lowers the lipid peroxidation marker TBARS when given in animal models of insulin resistance without fasting hyperglycemia, such as rats fed with high dosage of fructose.1 Previous studies have shown that rats fed with a high-fructose diet developed insulin resistance and hypertriglyceridemia,8 but not fasting hyperglycemia. This diet caused metabolic effects similar to those observed in syndrome X, in which insulin resistance, hypertension, and dyslipidemia are observed among patients with glucose intolerance.9 In the light of previous studies that showed the beneficial effects of antidiabetic agents on lipid peroxidation, the goal of the present study was to evaluate the TBARS-lowering capability of vanadyl sulfate in Wistar rats with insulin resistance.

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