Nonalcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis.

Research output: Contribution to journalArticle

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Abstract

Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.

Original languageEnglish
Pages (from-to)210-215
Number of pages6
JournalClinical and molecular hepatology
Volume19
Issue number3
Publication statusPublished - 2013 Sep 1

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Liver
Fatty Acids
Lipids
Lipogenesis
Incidence
Fatty Liver
Nonesterified Fatty Acids
Insulin Resistance
Non-alcoholic Fatty Liver Disease
Hepatocellular Carcinoma
Fibrosis
Obesity
Fats
Cholesterol
Glucose

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Nonalcoholic fatty liver disease : molecular mechanisms for the hepatic steatosis. / Koo, Seung-Hoi.

In: Clinical and molecular hepatology, Vol. 19, No. 3, 01.09.2013, p. 210-215.

Research output: Contribution to journalArticle

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