Abstract
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.
Highlights
In animals, high fructose diets cause multiple symptoms of metabolic syndrome such as insulinMetabolism of dietary fructose which occurs resistance (Thorburn et al, 1989)
The present study was designed to evaluate the amelioration of the inducible NOS (iNOS), Insulin Growth Factor-1 (IGF-1) genes expression and Insulin Receptor Substrate-1 (IRS-1) in liver tissues of rats fed high fructose diet treated with L-carnitine
The results revealed that feeding high fructose diet to rats induced significant elevation in iNOS and marked decreases in both IGF1mRNA and IRS-1 compared to those rats fed control diet studied
Summary
High fructose diets cause multiple symptoms of metabolic syndrome such as insulin. Insulin resistance is correlated with impaired insulin signaling This can involve dysfunction of cell surface components, such as Insulin Receptor (IR) as well as intracellular components like the insulin receptor substrate IRS-1 family of docking proteins and other elements of insulin signaling and glucose transport pathway Lamothe et al (1998). Increasing evidence indicates that Insulin Growth Factor-1 (IGF-1) protects against endothelial dysfunction, atherosclerotic plaque development and the metabolic syndrome (Conti et al, 2004). It promotes growth and differentiation in a variety of tissue (Baker et al, 1993). The present study was designed to evaluate the amelioration of the iNOS, IGF-1 genes expression and Insulin Receptor Substrate-1 (IRS-1) in liver tissues of rats fed high fructose diet treated with L-carnitine
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