Amelioration of Inducible Nitric Oxide Synthase, Insulin like Growth Factor-1 Gene Expression and Insulin Receptor Substrate-1 in Liver Tissue of Insulin Resistant Rats Treated With L-Carnitine

Problem statement: It has been reported that genes expression (inducible Nitric Oxide (iNOS). Insulin-like Growth Factor-1(IGF-1) have a role in both glucose homeostasis and insulin resistance. The aim of this study was designed to evaluate the amelioration of the iNOS, IGF-1 genes expression as well as IRS-1 in liver tissues of rats fed high fructose diet treated with Lcarnitine. Approach: About 24 male Wister rats of body weight 120-160 g were divided into 3 groups of 8 rats each. Group 1 received control diet, while group 2 and 3, rats received high fructose diet (60 g 100 g^-1 diet). Group 3, after 2 weeks from fructose feeding animals were treated with L-carnitine (CA) (300 mg kg^-1 body weight day^-1 i. p). At the end of the experimental period (30 days), serum levels of glucose, insulin, Triacylglycerol (TG) and cholesterol were determined. Hepatic contents of cholesterol, triacylglycerol, Malondialdehyde (MDA) and nitrogen oxide products were assayed. Genes expressions of iNOS, IGF-1 as well as IRS-1 were also determined in liver tissues of the experimental animals feeding high fructose diet. Results: Compared to control rats, the high fructose feeding in animals induces alterations in serum glucose, lipid metabolism and hepatic TG and MDA. In addition, fructose fed group develop marked increase in hepatic gene expression of iNOS and pronounced decreases in both IGF-1 mRNA and IRS-1 receptor. The administration of L-carnitine to rats fed high fructose diet mitigated the adverse effects of fructose load (insulin resistance) through the regulation of studied genes expression as well as insulin receptor substrate-1. Conclusion: The important findings of this context indicate the close association between hepatic gene expression (iNOS and IGF-1), IRS-1 receptor and insulin resistance. The exogenous CA to fructose fed rats improves the inflammation resulting from insulin resistance through the amelioration of the studied genes expression. This indicates that iNOS and IGF-1 have the characteristics to be marker of the metabolic syndrome.