Regulation of fat metabolism in the liver: link to non-alcoholic hepatic steatosis and impact of physical exercise

Regulation of fat metabolism in the liver: link to non-alcoholic hepatic steatosis and impact of... Hepatic steatosis may develop as a consequence of several dysfunctions. An increased circulating non-esterified fatty acid (NEFA) pool seems to be a major determinant in the pathogenesis of non-alcoholic fatty liver disease. Increased activation of the transcription factor sterol-regulatory-element-binding protein-1c, which promotes fatty acid synthesis, also contributes to hepatic fat accumulation. Increased hepatic fat oxidation with hepatic steatosis may be triggered by increased hepatic fat concentrations through the action of hepatic peroxisomes mediated by peroxisome proliferator-activated receptor α. Finally, inhibition in very low density lipoprotein secretion may also result in hepatic steatosis. This appears to be mainly controlled by the esterification of NEFAs into triacylglycerols by diacyglycerol acyltransferase-1 and −2 and the microsomal transfer protein. Physical exercise would interfere with the development of hepatic steatosis by stimulating lipid oxidation and inhibiting lipid synthesis in liver through the activation of the AMP-activated protein kinase pathway. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cellular and Molecular Life Sciences Springer Journals

Regulation of fat metabolism in the liver: link to non-alcoholic hepatic steatosis and impact of physical exercise

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Publisher
Springer Journals
Copyright
Copyright © 2006 by Birkhäuser Verlag, Basel
Subject
Life Sciences; Life Sciences, general; Biomedicine general; Biochemistry, general; Cell Biology
ISSN
1420-682X
eISSN
1420-9071
DOI
10.1007/s00018-006-6600-y
pmid
16649140
Publisher site
See Article on Publisher Site

Abstract

Hepatic steatosis may develop as a consequence of several dysfunctions. An increased circulating non-esterified fatty acid (NEFA) pool seems to be a major determinant in the pathogenesis of non-alcoholic fatty liver disease. Increased activation of the transcription factor sterol-regulatory-element-binding protein-1c, which promotes fatty acid synthesis, also contributes to hepatic fat accumulation. Increased hepatic fat oxidation with hepatic steatosis may be triggered by increased hepatic fat concentrations through the action of hepatic peroxisomes mediated by peroxisome proliferator-activated receptor α. Finally, inhibition in very low density lipoprotein secretion may also result in hepatic steatosis. This appears to be mainly controlled by the esterification of NEFAs into triacylglycerols by diacyglycerol acyltransferase-1 and −2 and the microsomal transfer protein. Physical exercise would interfere with the development of hepatic steatosis by stimulating lipid oxidation and inhibiting lipid synthesis in liver through the activation of the AMP-activated protein kinase pathway.

Journal

Cellular and Molecular Life SciencesSpringer Journals

Published: May 2, 2006

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