Prevention of high fructose-induced metabolic syndrome in male wistar rats by aqueous extract of Tamarindus indica seed

Tamarindus indica is used as a traditional treatment for diabetes. To elucidate whether Tamarindus indica seed aqueous extract [TSE] ameliorates metabolic syndrome in hyperinsulinemic rats, we evaluated serum insulin, dehydroepiandrosterone sulfate [DHEAS], triglyceride [TG], total cholesterol [TC], very low density lipoprotein [VLDL], low density lipoprotein [LDL], high density lipoprotein [HDL], and glucose levels in fructose-fed rats. Animals were divided into three groups; control [C] receiving tap water, fructose-fed [F] and TSE-treated fructose-fed rats [F-T] both receiving tap water supplemented with 10% [w/v] fructose. Water was prepared every day for a period of 8 weeks for all three groups. F-T rats were fed with TSE via gavage feeding at the dose of 20 mg/0.5 ml distilled water/100 g body weight per day. Fasting serum glucose levels of three groups were comparable. TSE treatment prevented the increase in fasting serum insulin, TG, TC, VLDL, and LDL in the F-T group [P<0.01] when comparing with the F group. Fructose feeding led to a decrease in fasting serum DHEAS, and HDL levels in the F group [P<0.01] compared with the control. TSE treatment prevented the decrease in fasting serum DHEAS, and HDL levels in the F-T group [P<0.01] while these results were not seen in control rats. It is indicated that the hyperinsulinemia in fructose-fed insulin resistant rats are associated with low levels of DHEAS, and HDL; and high levels of TC, VLDL, LDL, and TG. TSE supplementation probably ameliorates metabolic syndrome due to the improved insulin action

Low doses of vanadyl sulfate protect rats from lipid peroxidation and hypertriglyceridemic effects of fructose-enriched diet

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