PLA2G2D and obesity due to melanocortin 4 receptor deficiency: Mechanistically, sPLA2-IID hydrolyzes adipocyte-derived EVs to preferentially release ω3 PUFAs, which act on the PUFA receptor GPR120 to promote adipocyte browning and thermogenesis, thus counteracting diet-induced obesity, insulin intolerance, and hepatic steatosis (39, 40).