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Vitamin C and Vitamin E in Prevention of Nonalcoholic Fatty Liver Disease (NAFLD) in Choline Deficient Diet Fed Rats

DOI: 10.1186/1475-2891-2-9

Keywords: vitamin C, vitamin E, nonalcoholic fatty liver disease, oxidative stress

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Abstract:

Fatty liver disease was induced in Wistar rats by choline-deficient diet for four weeks. The rats were randomly assigned to receive vitamin E (n = 6) – (200 mg/day), vitamin C (n = 6) (30 mg/Kg/day) or vehicle orally.In the vehicle and vitamin E-treated rats, there were moderate macro and microvesicular fatty changes in periportal area without inflammatory infiltrate or fibrosis. Scharlach stain that used for a more precise identification of fatty change was strong positive. With vitamin C, there was marked decrease in histological alterations. Essentially, there was no liver steatosis, only hepatocellular ballooning. Scharlach stain was negative. The lucigenin-enhanced luminescence was reduced with vitamin C (1080 ± 330 cpm/mg/minx103) as compared to those Vitamin E and control (2247 ± 790; 2020 ± 407 cpm/mg/minx103, respectively) (p < 0.05). Serum levels of aminotransferases were unaltered by vitamin C or vitamin E.1) Vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by choline-deficient diet ; 2)Vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model.There are evidences that fatty liver, the most common hepatocellular change found in liver biopsies in humans, can play a role in the pathogenesis of chronic liver disease [1,2]. Recently, some authors have considered that a more accurate denomination for this disease, which encloses the whole spectrum of fatty liver, nonalcoholic steatohepatitis (NASH) and eventually cirrhosis, is Nonalcoholic Fatty Liver Disease (NAFLD) [3,4].Although several predisposing factors have been related to NAFLD, such as obesity, diabetes, jejunoileal bypass, dyslipidemia, drugs and parenteral nutrition, the pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease are still unclear [4]. As a consequence, the current treatment is largely conservative Some hypotheses have been implicated in the pathogenes

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