Hyperhomocysteinemia is a key for aggravation of liver injury in non-alcoholic fatty liver disease associated with cardiovascular disease in rats
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Abstract
Homocysteine has emerged as a novel independent marker of risk for the development of cardiovascular disease (CVD). Nonalcoholic fatty liver disease (NAFLD) is consistently associated with features of the metabolic syndrome, a condition carrying a high risk of cardiovascular events. The objective of this study was to investigate the correlation between non-alcoholic fatty liver and risk of cardiovascular disease. Also, this study evaluated the level of serum homocysteine and their association with the disease severity in rats fed high fructose diet. The obtained results revealed a significant (p<0.05) increase in carbohydrate profile (glucose, insulin & insulin resistance index) in NAFLD associated CVD rat groups dependent on the fructose intake as compared to their normal control ones. Lipid profile (cholesterol, triglycerides, HDL, LDL, VLDL & atherogenic index) were significantly (p<0.05) elevated in treated rats (fructose rat groups) when compared to their corresponding control group. Furthermore, liver profile (ALT, AST, GGT, L-FABP & haptoglobin) and cardiac profile (CK, LDH, H-FABP, myoglobin & homocystein) were significantly (p<0.05) increased throughout the whole experimental period in treated rats. The levels of inflammatory cytokines (CRP, TNF-?, IL-6 & IL-1?) were increased in animal groups which treated by fructose during the whole experimental periods (1, 2 & 3 months). On the other hand, NAFLD associated with CVD rats groups showed a significant (p<0.05) decrease in adiponectin level. These data suggested that high fructose diet induced NAFLD associated with CVD and confirmed the strict association between increased homocystein level, NAFLD and pronouncing of cardiovascular disease which reflected the degree of damage occur in both liver and heart.
How to Cite This Article
Heibashy, M.I.A. and Mazen, G.M.A. (2014); Hyperhomocysteinemia is a key for aggravation of liver injury in non-alcoholic fatty liver disease associated with cardiovascular disease in rats, International Journal of Advanced Research (IJAR), 2 (09), 0, ISSN 2320-5407.
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