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

摘要

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 insulinresistance. The aim of this study was designed to evaluate the amelioration of the iNOS, IGF-1genes 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 groupsof 8 rats each. Group 1 received control diet, while group 2 and 3, rats received high fructose diet (60 g100 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 ofglucose, insulin, Triacylglycerol (TG) and cholesterol were determined. Hepatic contents ofcholesterol, 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 theexperimental animals feeding high fructose diet. Results: Compared to control rats, the high fructosefeeding 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 andpronounced decreases in both IGF-1 mRNA and IRS-1 receptor. The administration of L-carnitine torats fed high fructose diet mitigated the adverse effects of fructose load (insulin resistance) through theregulation of studied genes expression as well as insulin receptor substrate-1. Conclusion: Theimportant 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 ratsimproves the inflammation resulting from insulin resistance through the amelioration of the studiedgenes expression. This indicates that iNOS and IGF-1 have the characteristics to be marker of themetabolic syndrome.