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.

Beta cell protective effects of sodium tungstate in streptozotocin-induced diabetic rats: glycemic control, blockage of oxidative stress and beta cell histochemistry.

BACKGROUND: Diabetes is a major public health problem. The development of new therapies that are able to improve glycemia management and even to cure diabetes is of great interest. In this study, protective effects of sodium tungstate against STZ-induced beta-cell damages were investigated. METHODS: Sixty rats were divided into six groups: control, diabetic, sodium tungstate treated diabetic rats from one week before STZ injection (TDB), food-restricted diabetic (FRD), tungstate treated control, sodium tungstate treated diabetic rats from one week after STZ administration (TDA). We evaluated serum insulin, glucose and glucose tolerance; liver glycogen content, glucokinase (GK) activity; blood and pancreas antioxidant power, lipid peroxidation; and fuchsin-aldehyde histochemical staining of beta-cells. RESULTS: Blood glucose levels of TDB group were lower than other diabetic groups (P<0.01). Blood insulin levels of all diabetic groups were lower than controls (P<0.01). Glucose intolerance improved in TDB animals. Blood and pancreas antioxidant power, liver glycogen contents and GK activities and granulated beta cells increased in TDB rats in comparison with other diabetic groups (P<0.01). Likewise, lipid peroxidation decreased significantly in TDB rats (P<0.01). CONCLUSIONS: Results suggested that sodium tungstate if administrated before STZ injection improves glycemic state by a direct effect on pancreatic beta-cells and preserves them by reducing the activity of these cells at the time of STZ injection, reducing STZ-induced oxidative stress, reducing insulin secretion, or all of the above mentioned.

Vanadyl sulfate ameliorates insulin resistance and restores plasma dehydroepiandrosterone-sulfate levels in fructose-fed, insulin-resistant rats.

OBJECTIVES: To elucidate whether vanadyl sulfate ameliorates the decreased dehydroepiandrosterone sulfate (DHEAS) in hyperinsulinemic rats, we evaluated plasma DHEAS, insulin and triglyceride (TG) levels in fructose-induced, insulin-resistant rats. DESIGN AND METHODS: Animals were divided into three groups: control (C), fructose fed (F-F), and vanadyl-treated fructose fed (F-T). Control animals were fed with standard chow; F-F and F-T groups fed with 66% fructose diet. F-F and C groups received tap water; F-T group received water supplemented with 0.2 mg/ml vanadyl sulfate. RESULTS: Fasting plasma glucose levels of three groups were comparable. Vanadyl treatment prevented the increase in plasma insulin and TG in the F-T group (P < 0.001) compared with the F-F group. Fructose feeding led to a decrease in plasma DHEAS in the F-F group (P < 0.001) compared with the C group. Vanadyl treatment prevented the decrease in plasma DHEAS in the F-T group (P < 0.001) compared with the F-F group. CONCLUSIONS: Our results indicated that the hyperinsulinemia in fructose-fed, insulin-resistant rats is associated with low levels of DHEAS. Vanadyl sulfate probably restores plasma DHEAS, due to the improved insulin action.