GPR52 accelerates fatty acid biosynthesis in a ligand-dependent manner in hepatocytes and in response to excessive fat intake in mice.

Gpr52 is an orphan G-protein-coupled receptor of unknown physiological function. We found that Gpr52-deficient ( ) mice exhibit leanness associated with reduced liver weight, decreased hepatic lipogenesis, and enhanced insulin sensitivity. Treatment of the hepatoma cell line HepG2 cells with c11, the synthetic GPR52 agonist, increased fatty acid biosynthesis, and GPR52 knockdown (KD) abolished the lipogenic action of c11.