期刊
MOLECULAR METABOLISM
卷 3, 期 5, 页码 565-580出版社
ELSEVIER
DOI: 10.1016/j.molmet.2014.04.010
关键词
Obesity; Hepatic steatosis; One-carbon metabolism; AMP-activated protein kinase; beta-oxidation; Acyl-carnitines
Non-alcoholic fatty liver disease (NAFLD) results from increased hepatic lipid accumulation and steatosis, and is closely linked to liver one carbon (C1) metabolism. We assessed in C57BL6/N mice whether NAFLD induced by a high-fat (HF) diet over 8 weeks can be reversed by additional 4 weeks of a dietary methyl-donor supplementation (MDS). MDS in the obese mice failed to reverse NAFLD, but prevented the progression of hepatic steatosis associated with major changes in key hepatic C1-metabolites, e.g. S-adenosyl-methionine and S-adenosylhomocysteine. Increased phosphorylation of AMPK-alpha together with enhanced beta-HAD activity suggested an increased flux through fatty acid oxidation pathways. This was supported by concomitantly decreased hepatic free fatty acid and acyl-carnitines levels. Although HF diet changed the hepatic phospholipid pattern, MDS did not. Our findings suggest that dietary methyl-donors activate AMPK, a key enzyme in fatty acid beta-oxidation control, that mediates increased fatty acid utilization and thereby prevents further hepatic lipid accumulation. (c) 2014 The Authors. Published by Elsevier GmbH.
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