Abstract
Chemerin (previously known as tazarotene-induced gene-2 or retinoic acid receptor responder-2) is an adipokine whose systemic levels are increased in human and rodent obesity [1-5]. Chemerin is an attractant for immune cells and may play a role in the recruitment of tissue macrophages [6]. This adipokine also regulates adipogenesis and glucose metabolism [2,7,8]. Chemerin is released as a proprotein with low biological activity, and extracellular C-terminal processing by distinct proteases generates bioactive polypeptides which exert proor antiinflammatory effects [6,7]. Hence, local and systemic levels of bioactive chemerin depend on proteolytic processing and are not simply related to chemerin protein concentrations determined by commercially available ELISAs or immunoblot techniques.
Highlights
Chemerin (previously known as tazarotene-induced gene-2 or retinoic acid receptor responder-2) is an adipokine whose systemic levels are increased in human and rodent obesity [1,2,3,4,5]
Chemerin is an adipokine whose systemic levels are increased in human and rodent obesity [1,2,3,4,5]
Chemerin is a ligand of the chemokine-like receptor 1 (CMKLR1) which is expressed by hepatocytes, hepatic stellate cells and Kupffer cells suggesting that chemerin affects liver cell function [11]
Summary
Chemerin (previously known as tazarotene-induced gene-2 or retinoic acid receptor responder-2) is an adipokine whose systemic levels are increased in human and rodent obesity [1,2,3,4,5]. IL-6 has, no effect on chemerin mRNA, cellular and soluble protein, and LPS does not increase chemerin protein in Primary Human Hepatocytes (PHH) [9,10]. FFA have no effect on chemerin mRNA and cellular protein levels in PHH while palmitate tends to lower chemerin in the respective supernatants [9,10].
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