Journal List > Korean J Gastroenterol > v.61(5) > 1007082

Jun: The Role of Diet in Nonalcoholic Fatty Liver Disease

Abstract

Prevalence of non-alcoholic fatty liver disease (NAFLD) is about 20–25% in Korean adults population. Obesity is strongly associated with NAFLD and the prevention of obesity is a major public issue. Unfortunately, pharmacological treatment of obesity and NAFLD remains uncertain. Only weight loss by dietary changes been shown to lead to histological improvement in fatty liver. So the nutrition therapy is a cornerstone of treatment for NAFLD. Epidemiologic studies show that saturated fat, trans-fatty acid, carbohydrate, and simple sugar have strong correlation with intrahepatic fat accumulation. But, true associations with specific nutrients still remain unclear. Recently, fructose consumption has been rising in many countries and several epidemiologic studies show that fructose consumption has strong correlation with metabolic diseases. The consumption of excessively added sugar in the pathogenesis of steatohepatitis has received attention. Most clinicians agree with lifestyle modification are effective in histologic improvement. Total energy intake restriction is the most important action to reduce intrahepatic fat accumulation. Macronutrient composition may also have correlation with the development of NAFLD. To reduce the incidence of NAFLD, public statements on optimal dietary education program have been issused. Various specific dietary programs are suggested. Among them low fat diet and low carbohydrate diet are suggested in patients with NAFLD. However, there is no ideal diet to obtain the histological improvement in NAFLD. Further randomised controlled studies about specific diet are needed to determine the long-term benefit and histological improvement by ideal diet. Tailoring diet therapy to a patient's lifestyle is more important than universal specific dietary program.

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Fig. 1.
Effects of fructose on pathogenesis of non-alcoholic fatty liver disease. PPAR-α, peroxisome proliferator-activated receptors-alpha; NASH, non-alcoholic steatohepatitis.
kjg-61-243f1.tif
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