KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARγ signaling.
KPV, an endogenous tripeptide, suppresses adipocyte differentiation and lipid accumulation in vitro by reducing ROS production and modulating AKT/mTOR/PPARγ signaling pathways. In a high-fat diet obesity mouse model, oral KPV administration reduced body weight gain, adipose tissue expansion, and obesity-related dyslipidemia including elevated cholesterol. These findings demonstrate KPV’s potential as a peptide-based therapeutic for obesity prevention and metabolic management, with clear mechanisms of action relevant to practitioner-prescribed metabolic support.