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Tumor 11ecrosis fnctor-alpha (TN F-a) has been suggested to play a key role in insulin resistance (/R), in obesity nnd may contribute to the development of lype 2 diabetes mellitus. £rythromyci11, one of tile macrolide muibiotics wns foHnd to exert various plrarmacological effects including suppression of TN F-a and other cytoki.11es levels as well as anrioxidam nctivity irr various slltdies i11 lwnwrr and animals. Tlw prese1;1 'sway was designed to investigale the be11ejicinl effect of erythromycin on insulin sensitivity in rMs fed ltiglz fructose diel. Albino rats of bot/1 sexes were divided inlo four groups containing /0 rats each. Control rats received the standard diet, while fructose fed rats received high fructose diet. Fmclose and erythromycin treated rats received high fructose diet and erythromyciu 40 111glkglday orally, while control and erythromy611 trealed rats 1 eceived sta11.dard diet cmd erythromycil/. After the treatme111 period of 30 days insulin resis((mce i11dex. by homeostasis model assessment ( HOMA) was determi11ed. The levels of lipid per-oxidntion. TN F-a a tid lipogmm were measured. Rats feeding lzighfruetose diet developed a significmu i11suli11 resismnce associated with increased TNF-a, lipid per-oxidation products. TG-LDL ami decrease in H DL and no change ill total cholesterol level. Administration of erythromycin to liigfl fmctose fed mrs produced beneficial effect on i'Jisulin sensitivity, dyslipidemin, TN F-a and lipid per-oxidation. A fall in TN F-a cotJCentrntion and lipid per-oxidation products by erytl!romycil1 sig11ify tiiC potentialtttilily of etylhromycill as an adjunct i.n treatment of insulin resi.stal/ce. 15 INTRODUCTION fed rats form a useful experimental model for insulin resis tance. Feeding rats with high fructose diet affects both glucose and lipid metabolism which result in d uster of metabolic abnormalities sLtch as glucose intolerance, hypertension, dyslipidemia and reduced insulin action (Dai et al.,l994) thus fructoseMa:1sou rn f. Fore11s ic Med. Cli11 . Toxicol. Tumor necrosis factor-alpha (TNF-a.) is a peptide constitutively expressed and secreted by adipose tissue (Erosy e t al., 2004). It has been demonstr<1 ted th<1t Tl\IFa, may be a media tor of insulin resistance Vol. XII No. 1, famta nJ 2005

Effect of Erythromycin on Insulin Resistance and Tumour Necrosis Factor-Alpha Levels in Fructose Fed Insulin Resistant Rats