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TUG‐891, an agonist of GPR120, inhibits lipid accumulation in hepatocytes
Author(s) -
Park Soojin,
Kang Saeromi,
Im Dongsoon
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.992.5
Subject(s) - gpr120 , polyunsaturated fatty acid , fatty liver , steatosis , medicine , receptor , endocrinology , free fatty acid receptor 1 , agonist , hepatic stellate cell , chemistry , fatty acid , biology , biochemistry , g protein coupled receptor , disease
Background Omega‐3 polyunsaturated fatty acids have protective functions on non‐alcoholic fatty liver disease. Recently, a G protein‐coupled receptor named GPR120 was identified as a receptor for omega‐3 polyunsaturated fatty acids and its protective functions in insulin resistance and hepatic steatosis. Also, GPR120 expression in hepatocytes has also been shown from liver biopsies from child fatty liver disease patients. METHODS In order to assess functional roles of GPR120 in hepatocytes, an in vitro model of liver X receptor‐mediated hepatocellular steatosis was used. RESULTS GPR120 expression was confirmed in human hepatoma cells. A specific liver X receptor activator induced lipid accumulation and TUG‐891, an agonist of GPR120, inhibited the lipid accumulation. TUG‐891‐induced inhibition was ameliorated by treatment of siRNA transfection of GPR120 or AH7614 (GPR120 antagonist) treatment. SREBP‐1c, a key transcription factor for lipogenesis, was induced by liver X receptor activation. The SREBP‐1c induction was also inhibited by TUG‐891 at mRNA and protein levels. TUG‐891‐induced suppression of SREBP‐1c expression was again blunted by GPR120‐knockdown in the hepatocytes. Therefore, the present data suggest that GPR120 in hepatocytes may function as a receptor for omega‐3 polyunsaturated fatty acids to protect lipid accumulation in the liver. CONCLUSION Protective functions of omega‐3 polyunsaturated fatty acids on non‐alcoholic fatty liver disease may be mediated by interaction with GPR120 in hepatocytes.