exposure to HFD. However, FoxO1 KODAT mice showed improved glucose tolerance both in NC and HFD compared with WT mice. These results imply that mild activation of BAT in the FoxO1 KODAT mice under NC diet or acute HFD exposure might primarily enhance lipid oxidative metabolism, which eventually led to improved whole-body glucose homoeostasis. However, prolonged activation of BAT under chronic HFD exposure might also contribute to glucose clearance and result in further improved glucose tolerance and body weight in the FoxO1 KODAT mice. Subsequently, the improved glucose metabolism in FoxO1 KODAT mice might be also attributed to the decreased body weight under HFD condition. Altogether, these data strongly indicate that increased thermogenesis and energy expenditure might be the major cause of the metabolic phenotypes observed in FoxO1DAT KO mice.
