Journal
NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
Volume 19, Issue 4, Pages 291-302Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.numecd.2008.12.015
Keywords
Fatty liver; Insulin; Metabolic syndrome; Hepatic lipid; metabolism; Microsome; Peroxidation; Gene expression; Lipoprotein export; Metformin; Apoptosis
Funding
- University of Padova
- PhD program of Fondazione Cassa di Risparmio di Padova e Rovigo, Italy
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Non-alcoholic fatty liver disease (NAFLD) is an increasingly recognized pathology with a high prevalence and a possible evolution to its inflammatory counterpart (non-alcoholic steatohepatitis, or NASH). The pathophysiology of NAFLD and NASH has many links with the metabolic syndrome, sharing a causative factor in insulin resistance. According to a two-hit hypothesis, increased intrahepatic triglyceride accumulation (due to increased synthesis, decreased export, or both) is followed by a second step (or hit), which may lead to NASH. The tatter likely involves oxidative stress, cytochrome P450 activation, lipid peroxidation, increased inflammatory cytokine production, activation of hepatic stellate cells and apoptosis. However, both hits may be caused by the same factors. The aim of this article is to overview the biochemical steps of fat regulation in the liver and the alterations occurring in the pathogenesis of NAFLD and NASH. (c) 2009 Elsevier B.V. All rights reserved.
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