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Low doses of vanadyl sulfate protect rats from lipid peroxidation and hypertriglyceridemic effects of fructose-enriched diet
International Journal of Diabetes and Metabolism. 2006; 14 (3): 134-137
Dans Anglais | IMEMR | ID: emr-128052
ABSTRACT
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 fructoseenriched diet that leads to insulin resistance. 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. 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. 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
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Indice: Méditerranée orientale langue: Anglais Texte intégral: Int. J. Diabetes Metab. Année: 2006

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Indice: Méditerranée orientale langue: Anglais Texte intégral: Int. J. Diabetes Metab. Année: 2006