Although the precise mechanisms of LEAP2-mediated feeding regulation so far remain unclear, it is likely that LEAP2 exerts its antiorexigenic effects most prominently in an overnutrition state, and this assessment is supported by a disrupted LEAP2/ghrelin balance toward an increased LEAP2/ghrelin molar ratio in obese participants with a BMI higher than 30 kg/m2 and a postprandial LEAP2 elevation in obese women but not in those within a normal BMI range (32). This evidence concerns the gene LEAP2 and overnutrition.