Key result
Administration of the CMKLR1 antagonist α-NETA suppressed serum TC, TG, AST, ALT levels, and hepatic TG content in a mouse model of high-fat-diet-induced fat accumulation.
The CMKLR1 antagonist α-NETA reduces diet-induced fat accumulation and improves lipid profiles in preclinical models of NAFLD.
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α-NETA attenuates steatosis in mice; hypothesis-generating for CMKLR1 antagonism in human NAFLD, no practice change yet.
Objective: Non-alcoholic Fatty Liver Disease (NAFLD) is believed to be correlated with chemerin and its receptor, Chemokine-like Receptor 1 (CMKLR1).We analyse the role of CMKLR1 in NAFLD by using a novel small molecule CMKLR1 antagonist-NETA (2-naphthoyl ethyl trimethyl ammonium) in vitro and in vivo. Methods:We assessed the effects of -NETA on a mouse model of high-fat-diet-induced fat accumulation in liver and adipose tissue and an analogous cell model established by culturing Hepa 1-6 and 3T3-L1 cells.Results: We found that chemerin and CMKLR1 mRNA were significantly increased in the livers and fat tissue of the mice fed the high fat diet relative to those in mice fed the normal diet.α-NETA administration suppressed serum TC, TG, AST and ALT levels and hepatic TG content as well as inhibited lipid metabolism-associated factors in the livers and fat of high fat diet mice.Furthermore, in the cell model, α-NETA suppressed oleic acid induction of Hepa 1-6 cell steatosis, 3T3-L1 adipogenesis and the expression of mRNAs for related lipid metabolism-associated factors.Conclusions: Chemerin/CMKLR1 signaling plays an important role in the progression of NAFLD.
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Zhang et al. (2018) studied Non-alcoholic Fatty Liver Disease (NAFLD). α-NETA (2-naphthoyl ethyl trimethyl ammonium) vs. Normal diet / untreated was evaluated on Serum TC, TG, AST, ALT levels, hepatic TG content, and lipid metabolism-associated factors. Administration of the CMKLR1 antagonist α-NETA suppressed serum TC, TG, AST, ALT levels, and hepatic TG content in a mouse model of high-fat-diet-induced fat accumulation.
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