The Role of Diet and Nutrient Composition in Nonalcoholic Fatty Liver Disease

      Abstract

      Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the developed world. NAFLD is tightly linked to insulin resistance and considered to be the hepatic manifestation of the metabolic syndrome. The cornerstone of any treatment regimen for patients with NAFLD is lifestyle modification focused on weight loss, exercise, and improving insulin sensitivity. Here we review the literature and discuss the role of diet and nutrient composition in the management of NAFLD. Because there are currently no specific dietary guidelines for NAFLD, this review proposes a dietary framework for patients with NAFLD based on the available evidence and extrapolates from dietary guidelines aimed at reducing insulin resistance and cardiovascular risk.

      Keywords

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      Biography

      E. M. McCarthy is a registered dietitian, Northwestern Faculty Foundation, Chicago, IL.

      Biography

      M. E. Rinella is an associate professor of medicine, Department of Gastroenterology and Hepatology, Northwestern University Feinberg School of Medicine, Northwestern Memorial Hospital, Chicago, IL.

      Linked Article

      • Dietary Intervention in Non-Alcoholic Fatty Liver Disease
        Journal of the Academy of Nutrition and DieteticsVol. 113Issue 2
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          In a recent review by McCarthy and Rinella,1 the authors reported that in non-alcoholic fatty liver disease (NAFLD) patients' early identification and treatment could prevent the development of cirrhosis and its complications. The prevalence of NAFLD in industrialized countries is about 30%.2 It has been reported that insulin resistance, type 2 diabetes mellitus, dyslipidemia, and obesity are the central risk factors for NAFLD development. In particular, visceral adipose tissue has an important role in the secretion of several adipokines and cytokines involved in the underlying fat accumulation mechanisms, hepatocyte injury and apoptosis, neutrophil chemotaxis, and hepatic stellate cell activation.
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