Our study pertains to the potential ability of vitamin C and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress induced by cadmium. Male rats were randomly divided into five groups of eight each. Group I served as the controls; group II received in their drinking water CdCl 2 (200 mg/L); group III received both CdCl 2 and vitamin C (1.5 g/L of water); group IV was treated with CdCl 2 and vitamin E (400 mg/kg diet); and group V received CdCl 2 + vitamin C + vitamin E. The exposure of rats to cadmium chloride for 30 days resulted in a significant decrease in body weight gain. Cadmium treatment also produced oxidative liver injury characterized by increasing serum glucose concentration, glutamate-pyruvate transaminase (GPT), alanine aminotransaminase (GOT) and alkaline phosphatase (ALP) activities. Meanwhile cadmium supplementation decreased serum total protein and albumin in animals. In addition, liver glutathione level, catalase and glutathione peroxidase (GSH-Px) activities were diminished. With vitamin C and vitamin E administration during intoxication of cadmium, corrective effects on Cd-induced oxidative stress in the liver was observed. In conclusion, this study demonstrates that oral exposure to Cd caused reduction in LPO and antioxidant enzyme activities in rat's liver, and vitamin C or vitamin E may have partial ameliorative effects on these disturbances, whereas vitamin C and vitamin E together assured a more efficient protection of the organ against the noticed oxidative stress.
The aim of this study was to investigate the beneficial effect of vitamin E supplementation on zinc deficiency in experimental diabetes. Male alloxan-diabetic Wistar, albino rats of 10 weeks of age were divided into three groups. The first group received a diet containing 54 mg zinc/kg (adequate zinc group, AZ), the second group received a diet containing 1mg zinc/kg (zinc deficient group, ZD), and the third group received a diet containing 1mg zinc/kg supplemented with vitamin E (500mg/kg diet) (ZD+VE). Body weight gain and food intake of all rats were recorded regularly over a period of four weeks. On day 28, after overnight fasting, animals were killed and blood glucose, serum cholesterol, serum triglycerides, serum protein, serum urea, serum zinc, femur zinc, pancreatic zinc, testis zinc, liver glutathione concentrations and serum glutamic oxalic transaminase (GOT), serum glutamic pyruvic transaminase (GPT) and serum alkaline phosphatase activities were determined on blood and tissue samples. Body weight gain of zinc deficient diabetic animals at the end of four weeks of dietary manipulation was significantly lower than that of zinc adequate diabetic animals. Dietary zinc intake significantly increased blood glucose, serum cholesterol, serum triglycerides, and serum urea of zinc deficient diabetic rats. In contrast, serum zinc, femur zinc, pancreatic zinc, serum protein and liver glutathione levels were lower. The consumption of zinc deficient diet led also to an increase in serum GOT, GPT coupled with a decrease in serum alkaline phosphatase. Vitamin E ameliorated all the previous parameters. In conclusion, the present study demonstrates that vitamin E supplementation significantly reduced the severity of zinc deficiency in diabetes mellitus. (Int J Diabetes Metab 15: 46-50, 2007)
Chronic kidney disease (CKD) is associated with a large range of metabolic alterations among which insulin resistance and dyslipidemia. We hypothesize that a phenomenon of lipotoxicity and ectopic fat redistribution could be responsible for the insulin-resistance associated to CKD. C57BL/6 mice underwent a 5/6 nephrectomy and were compared to pair fed sham-operated mice. Insulin sensitivity was estimated through intra-peritoneal insulin (ipITT) and glucose tolerance (ipGTT) tests. Anthropometric (body weight, lean and fad pad mass) and metabolic parameters (glycemia, insulin, cholesterol, triglycerides) were measured. The phosphorylation of a key protein of insulin signaling pathway (protein kinase B, PKB/Akt) was studied by Western blot. The intra-muscular and intra-hepatic lipids were extracted using Chloroform-Methanol (2:1, v/v).The CKD mice exhibited a marked decrease in insulin sensitivity (À 76%, po0.01) and altered glucose tolerance (þ24%, po0.001). CKD mice exhibited a profile of insulin resistance. CKD mice exhibited a significant decrease in white adipose tissue accretion (À 57%, po 0.001) associated with increased muscle (þ138%, po0.05) and liver (þ 38%, Po0.05) lipid contents compared to sham-operated mice. The CKD mice presented a blunted insulin-induced Akt phosphorylation (À 34%, po0.05) in gastrocnemius muscle.In subtotally nephrectomized mouse model we showed an ectopic intramuscular and intrahepatic lipid redistribution concomitant with insulin resistance. Insulin resistance and lipotoxicity may represent the missing links (beyond the classical cardiovascular risk factors) that may help explain the increased risk of cardiovascular disease in CKD.http://dx.
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