Chemerin in Liver Diseases

Chemerin is a chemoattractant protein and moreover has a role in adipogenesis, angiogenesis and glucose homeostasis. Chemerin is primarily synthesized and secreted by adipocytes and hepatocytes. Chemerin receptors chemokine-like receptor 1 (CMKLR1), G-protein coupled receptor 1 (GPR1) and CC-motif chemokine receptorlike 2 (CCRL2) are all expressed in the liver suggesting that chemerin may be relevant in liver physiology and pathophysiology. Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and is the most common cause of chronic liver injury. NAFLD and chronic hepatitis C virus infection are risk factors for hepatocellular carcinoma. Hepatic and serum chemerin have been analyzed in human and rodent NAFLD, in patients with chronic hepatitis C and patients with hepatocellular carcinoma. Chemerin, GPR1 and CMKLR1 deficient mice have been used to elucidate the role of these proteins in body weight gain and glucose homeostasis. The regulation of chemerin and CMKLR1 by adipokines, hormones and cytokines relevant in liver diseases has been studied in hepatocytes. The data published so far are briefly summarized herein. Current experimental findings do not provide evidence for a crucial role of chemerin in chronic liver diseases and further research is needed to evaluate a possible protective function of this protein in hepatocellular carcinoma. *Corresponding author: Christa Buechler, PhD, Department of Internal Medicine I, Regensburg University Hospital, 93042 Regensburg, Germany, Tel: +49-941-9447009; Fax: +49-941-944-7019; E-mail: [email protected] Received September 25, 2014; Accepted November 14, 2014; Published November 19, 2014 Citation: Buechler C (2014) Chemerin in Liver Diseases. Endocrinol Metab Synd 3: 144. doi:10.4172/2161-1017.1000144 Copyright: © 2014 Buechler C. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.