Chemerin is highly expressed in hepatocytes and is induced in non-alcoholic steatohepatitis liver


Chemerin is a recently described adipokine whose adipose tissue and serum levels are increased in obesity. Chemerin is expressed in the liver, and here, expression of chemerin has been studied in liver cells and in non-alcoholic fatty liver disease (NAFLD) which is more often found in obesity. Chemerin is shown to be highly expressed in primary human hepatocytes (PHH) whereas hepatic stellate cells (HSC) produce only low levels of this protein. In mice fed a high fat diet hepatic chemerin mRNA but not protein is increased. Chemerin protein is comparably expressed in the liver of control animals and ob/ob mice. Rodents fed a Paigen diet or methionine-choline deficient diet (MCD) develop non-alcoholic steatohepatitis (NASH), and liver chemerin protein tends to be higher in the first and is significantly increased in the latter. Of note, MCD fed mice have similar serum chemerin levels as the respective control animals despite lower body weight. In human fatty liver and NASH liver chemerin mRNA also tends to be induced. Cytokines like TNF and adipokines with an established role in NASH do not considerably affect PHH chemerin protein. The antidiabetic drug metformin reduces cellular and soluble chemerin in PHH as has already been described in adipose tissue. In conclusion current data show that primary human hepatocytes are a major source of hepatic chemerin and increased liver chemerin in NASH may even contribute to systemic levels.


Projects: A1.1: Central liver metabolism and its regulation under nutritional chal..., A3.6: Transcription factor network and links to metabolism in NAFLD, CTU SOP Human Hepatocytes, Show cases

Exp. Mol. Pathol.
Exp. Mol. Pathol. 95(2): 199-205
29th Jul 2013

Sabrina Krautbauer, Josef Wanninger, Kristina Eisinger, Yvonne Hader, Michael Beck, Andrea Kopp, Andreas Schmid, Thomas S Weiss, Christoph Dorn, Christa Buechler

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[Thomas Weiss]

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Cell and Liver
Views: 1735
  • Created: 30th Jan 2014 at 17:11

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