Journal of Gastrointestinal & Digestive System
Open Access

Review Article

High-fructose Intake in Obesity-related Nonalcoholic Fatty Liver Disease

Geyza NA Armiliato, Silvia M Ferolla^*, Teresa CA Ferrari and Cláudia A Couto

Department of Internal Medicine, School of Medicine, Universidade Federal de Minas Gerais, Belo Horizonte 30130-100, Brazil

*Corresponding Author:

Silvia M. Ferolla
Department of Internal Medicine, School of Medicine
Universidade Federal de Minas Gerais
Belo Horizonte 30130-100, Brazil
Tel: +55-31-3409-9746
Fax: +55-31-3409-9664
E-mail: contato@silviaferolla.com.br

Received date: March 17, 2015; Accepted date: April 11, 2015; Published date: April 20, 2015

Citation: Armiliato GNA, Ferolla SM, Ferrari TCA, Couto CA (2015) High-fructose Intake in Obesity-related Nonalcoholic Fatty Liver Disease. J Gastrointest Dig Syst 5:281. doi:10.4172/2161-069X.1000281

Copyright: © 2015 Armiliato GNA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. NAFLD involves a spectrum of conditions that include pure steatosis without inflammation, nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis. Insulin resistance (IR) plays a main role in the pathophysiology of NAFLD by causing lipid accumulation in the hepatocytes, which may be followed by lipid peroxidation, production of reactive oxygen species and consequent inflammation. The consumption of carbohydrates, particularly sugars additives high in fructose increased dramatically in the past decades and appears to be at least one very important contributing factor in NAFDL pathogenesis. Recent studies suggest that the excessive consumption of fructose from sugar additives (mainly those found in sweetened beverages and processed foods) is linked to development and severity of NAFLD by induction of IR, postprandial hypertriglyceridemia and lipid accumulation in the liver, especially in individuals with overweight. We discuss the possible mechanisms involving fructose consumption, lipid accumulation and development of NASH. This review also presents the chief findings from all the studies that evaluated fructose consumption in human NAFLD.

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