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-a) exerts a partial role in 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 vatsar-tan (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+ sa-
line), (FFR+ saline), (Standard diet + metformin), (FFR+ metformin), (stan­dard diet+ valsartan) and (FFR+ val-sartan). In all rats, body weight, fast­ing serum glucose, fasting serum insulin, insulin sensitivity test, fasting glucose insulin ratio (FGIR), serum TNF-a and serum malondiaidehyde (MDA) were measured. Results 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-a and MDA. It could be con­cluded that TNF-a and angiotensin II might regulate insulin sensitivity in non-obese FFR.