Characterization of the metabolic phenotypes in the offspring at birth and in adulthood, under normal and high-fat diet (HFD) conditions, revealed an increased susceptibility to obesity and glucose homeostasis dysfunction in the adult offspring that experienced loss of placental mTOR (CYP19Cre+ mTORfl/fl, hereafter mTOR-KOPlacenta), whereas gain of placental mTORC1 activity conferred protection under metabolic stress. Here, MTOR is linked to obesity disorder.