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Mansoura Medical Journal. 2006; 37 (1-2): 363-379
in English | IMEMR | ID: emr-182176

ABSTRACT

Insulin resistance [IR] is a consequence of high fructose fed diet in rats. The current study was carried out to declare if tumor necrosis factor alpha [TNF-alpha] exerts a partial role the development of IR in non-obese rat model; fructose fed rats [FFR] like that happens in obese rat models. We evaluate the influence of valsartan [a selective blocker of angiotensin receptor type-1] in comparison to metformin [a known insulin sensitizer] on enhancement of insulin sensitivity in FFR. Rats were divided into 2 equal groups [36 rats /group], one group received high fructose diet to induce insulin resistance and the other included standard diet fed rats. Each group is further divided into 3 equal subgroups, [standard diet+ saline], [FFR+ saline], [Standard diet + metformin], [FFR+ metformin]. [Standard diet+ valsartan] and [FFR+ valsartan]. In all rats, body weight, fasting serum glucose, fasting serum insulin, insulin sensitivity test, fasting glucose insulin ratio [FGIR], serum TNF-alpha and serum malondialdehyde [MDA] were measured. Result revealed that administration of valsartan to FFR produced a comparable improvement of insulin resistance. In addition valsartan treatment in FFR produced significant decrease in serum TNF-alpha and MDA. It could be concluded that TNF-alpha and angiotensin II might regulate insulin sensitivity in non-obese FFR


Subject(s)
Male , Animals, Laboratory , Fructose , Malondialdehyde/blood , Tumor Necrosis Factor-alpha/blood , Mice, Inbred NOD/blood , Valine/blood , Receptor, Angiotensin, Type 1 , Metformin , Rats
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