Data from: Medium-chain fatty acid receptor GPR84 deficiency leads to metabolic homeostasis dysfunction in mice fed high-fat diet

Overconsumption of food, especially dietary fat, leads to metabolic
disorders such as obesity and type 2 diabetes. Long-chain fatty acids,
such as palmitoleate are recognized as the risk factors for these
disorders owing to their high-energy content and lipotoxicity. In
contrast, medium-chain fatty acids (MCFAs) metabolic benefits; however,
their underlying molecular mechanisms remain unclear. GPR84 is an MCFA
receptor, particularly for C10:0. Although evidence from in vitro
experiments and oral administration of C10:0 in mice suggests that GPR84
is related to the metabolic benefits of MCFAs via glucose metabolism, its
precise roles in vivo remain unclear. Therefore, the present study
investigated whether GPR84 affects glucose metabolism and metabolic
function using Gpr84-deficient mice. Although Gpr84-deficient mice were
lean and had increased endogenous MCFAs under HFD feeding conditions, they
exhibited hyperglycemia and hyperlipidemia along with lower plasma insulin
and glucagon-like peptide-1 (GLP-1) levels compared with wild-type mice.
Medium-chain triglyceride (C10:0) intake suppressed obesity, and improved
plasma glucose and lipid levels, and increased plasma GLP-1 levels in
wild-type mice; however, these effects were partially attenuated in
Gpr84-deficient mice. Our results indicate that long-term MCFA-mediated
GPR84 activation improves the dysfunction of glucose and lipid
homeostasis. Our findings may be instrumental for future studies on drug
development with GPR84 as a potential target, thereby offering new avenues
for the treatment of metabolic disorders like obesity and type 2 diabetes.