HCAR2 and diabetes mellitus: Since β-HB is generated in the liver from fatty acid oxidation following fat mobilization from adipocytes, it is believed that β-HB, through its interaction with GPR109A present on adipocytes, may inhibit triglyceride hydrolysis and release of free fatty acids as a negative feedback regulatory mechanism, promoting the maintenance of metabolic homeostasis during conditions such as starvation and diabetes [8].