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J Clin Biochem Nutr. 2012 Nov;51(3):163-9. doi: 10.3164/jcbn.12-06. Epub 2012 Jun 8.

Analysis of vanin-1 upregulation and lipid accumulation in hepatocytes in response to a high-fat diet and free fatty acids.

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1
Department of Microbiology and Immunochemistry, Asahikawa Medical College, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, Hokkaido 078-8510, Japan.

Abstract

High-fat diet is one of the causes of nonalcoholic fatty liver disease. We have previously demonstrated that high-fat diet induces upregulation of adipose differentiation-related protein mRNA expression accompanied by lipid droplet formation in mouse liver. Vanin-1 is a ubiquitous epithelial ectoenzyme that has pantetheinase activity and produces cysteamine, a potent endogenous antioxidant. In the present study, we analyzed the expression of hepatic vanin-1 mRNA following the administration of a high-fat diet in mice as well as free fatty acids in hepatocyte cultures and speculated its possible mechanism. Vanin-1 mRNA levels in the livers of mice were upregulated within a day of the high-fat diet, even before the expression of adipose differentiation-related protein mRNA and lipid accumulation. An in vitro analysis using HuH-7 cells revealed a significant upregulation of vanin-1 mRNA by as low as 0.01 mM oleic acid; however, lipid accumulation in hepatocytes was not affected at this concentration. Furthermore, vanin-1 mRNA was differentially upregulated by various free fatty acids irrespective of the grade of lipid accumulation. These findings indicate that the upregulation of vanin-1 precedes lipid accumulation and is differentially mediated by various types of free fatty acids in the model, presenting vanin-1 as a novel player in the pathogenesis of nonalcoholic fatty liver disease.

KEYWORDS:

fatty acids; lipid droplet; nonalcoholic fatty liver disease; vanin-1

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