Adiponectin upregulates hepatocyte CMKLR1 which is reduced in human fatty liver

Wanninger, Josef and Bauer, Sabrina and Eisinger, Kristina and Weiss, Thomas S. and Walter, Roland and Hellerbrand, Claus and Schaeffler, Andreas and Higuchi, Akiko and Walsh, Kenneth and Buechler, Christa (2012) Adiponectin upregulates hepatocyte CMKLR1 which is reduced in human fatty liver. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 349 (2). pp. 248-254. ISSN 0303-7207,

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Abstract

Chemokine-like receptor 1 (CMKLR1) ligands chemerin and resolvin El are suggested to have a role in non-alcoholic fatty liver disease (NAFLD). Here, expression of CMKLR1 in liver cells and NAFLD was studied. CMKLR1 was detected in primary human hepatocytes (PHH), Kupffer cells, bile-duct cells and hepatic stellate cells. In human and rodent fatty liver and in fibrotic liver of mice fed a methionine-choline deficient diet CMKLR1 was reduced. Hepatocytes are the major cells in the liver and effects of adipokines, cytokines and lipids on CMKLR1 in PHH were analyzed. Increased cellular triglyceride or cholesterol content, lipopolysaccharide, IL-6, TNF and leptin did not influence CMKLR1 levels in PHH whereas profibrotic TGF beta tended to reduce CMKLR1. Adiponectin strongly upregulated CMKLR1 mRNA and protein in PHH and hepatic CMKLR1 when injected into wild type mice. Further, CMKLR1 was suppressed in the liver of adiponectin deficient mice. These data indicate that low CMKLR1 in NAFLD may partly result from reduced adiponectin activity. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

Item Type: Article
Uncontrolled Keywords: NONALCOHOLIC STEATOHEPATITIS; INSULIN-RESISTANCE; KNOCKOUT MICE; METABOLIC SYNDROME; HEPATIC STEATOSIS; RECEPTOR CHEMR23; ADIPOSE-TISSUE; RESOLVIN E1; CHEMERIN; CELLS; Adipokine; Hepatic steatosis; Chemerin receptor; Liver
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Medicine > Lehrstuhl für Kinder- und Jugendmedizin
Depositing User: Dr. Gernot Deinzer
Date Deposited: 19 May 2020 06:52
Last Modified: 19 May 2020 06:52
URI: https://pred.uni-regensburg.de/id/eprint/19217

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