Loss of GPR109A/HCAR2 induces aging-associated hepatic steatosis.

ABSTRACT: GPR109A agonists have been used for the treatment of obesity however, the role of GPR109A in regulating aging-associated alterations in lipid metabolism is unknown. In this study we used Gpr109a^-/- mice to investigate the effect of aging in the regulation of lipid accumulation. We observed that in mouse and human livers, in addition to Kupffer cells, GPR109A is expressed in hepatocytes. Over 12 months, compared to wild type (WT), Gpr109a^-/- mice gained significantly more weight. Food intake and levels of serum lipids were similar among both groups. Compared to age-matched WT mice, 12-months old Gpr109a^-/- mice had significantly increased liver weight, hepatic steatosis and serum markers of liver injury. The fatty liver phenotype in G

SUBMITTER: Jadeja RN 

PROVIDER: S-EPMC6366969 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature