HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Tables All Versions of this Article: 294/5/G1281    most recent 00074.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Greco, D. Articles by Yki-Järvinen, H. Search for Related Content PubMed PubMed Citation Articles by Greco, D. Articles by Yki-Järvinen, H.

LIVER AND BILIARY TRACT

Gene expression in human NAFLD

¹Institute of Biotechnology, University of Helsinki; ²Department of Medicine, Division of Diabetes, University of Helsinki; ³Minerva Medical Research Institute, Helsinki; ⁴Department of Medicine, Division of Gastroenterology, University of Helsinki; and ⁵Department of Surgery, University of Helsinki, Helsinki, Finland; and ⁶Atherosclerosis Research Unit, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden

Submitted 14 February 2008 ; accepted in final form 1 April 2008

Despite the high prevalence of nonalcoholic fatty liver disease (NAFLD), little is known of its pathogenesis based on study of human liver samples. By the use of Affymetrix GeneChips (17,601 genes), we investigated gene expression in the human liver of subjects with extreme steatosis due to NAFLD without histological signs of inflammation (liver fat 66.0 ± 6.8%) and in subjects with low liver fat content (6.4 ± 2.7%). The data were analyzed by using sequence-based reannotation of Affymetrix probes and a robust model-based normalization method. We identified genes involved in hepatic glucose and lipid metabolism, insulin signaling, inflammation, coagulation, and cell adhesion to be significantly associated with liver fat content. In addition, genes involved in ceramide signaling (MAP2K4) and metabolism (UGCG) were found to be positively associated with liver fat content. Genes involved in lipid metabolism (PLIN, ACADM), fatty acid transport (FABP4, CD36), amino acid catabolism (BCAT1), and inflammation (CCL2) were validated by real-time PCR and were found to be upregulated in subjects with high liver fat content. The data show that multiple changes in gene expression characterize simple steatosis.

liver fat; nonalcoholic fatty liver disease; lipid metabolism; inflammation; ceramides

This article has been cited by other articles:

				E. Fabbrini, F. Magkos, B. S. Mohammed, T. Pietka, N. A. Abumrad, B. W. Patterson, A. Okunade, and S. Klein Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity PNAS, September 8, 2009; 106(36): 15430 - 15435. [Abstract] [Full Text] [PDF]

				M. You and C. Q. Rogers Adiponectin: A Key Adipokine in Alcoholic Fatty Liver Experimental Biology and Medicine, August 1, 2009; 234(8): 850 - 859. [Abstract] [Full Text] [PDF]

				R. L. Silverstein and M. Febbraio CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior Sci. Signal., May 26, 2009; 2(72): re3 - re3. [Abstract] [Full Text] [PDF]