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Nutr Metab Cardiovasc Dis. 2009 May;19(4):291-302. doi: 10.1016/j.numecd.2008.12.015. Epub 2009 Apr 8.

Hepatic lipid metabolism and non-alcoholic fatty liver disease.

Author information

1
Department of Clinical and Experimental Medicine, Chair of Metabolism, University of Padua, Italy. paolo.tessari@unipd.it

Abstract

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 latter 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.

PMID:
19359149
DOI:
10.1016/j.numecd.2008.12.015
[Indexed for MEDLINE]

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