Ampka2 deficiency does not affect the exercise-induced improvements in glucose tolerance and metabolic disorders in mice fed a high-fat diet

Abstract

Exercise can improve obesity and metabolic disorders in mice fed a high-fat diet (HFD), but the role of AMPKa2 in the process remains unclear. The aim of this study was to investigate the role of AMPKa2 in the exercise-induced improvements in glucose tolerance and metabolic turnover in obesity mice. Male wild-type mice (n512) and AMPKa2 knockout (AMPKa2 KO) mice (n512) were fed a HFD for 16 wk and were then randomly divided into four groups: WT HFD group (WT HF), AMPKa2 KO HFD group (AMPKa2 KO HF), WT HFD exercise group (WT HE), and AMPK HFD exercise group (AMPKa2 KO HE). The HF groups continue to be fed a HFD from 16 wk to 24 wk, and the HE groups were fed a HFD and performed exercise training. After 8 wk of exercise, all mice were placed in an energy metabolism chamber to test their metabolic turnover, include locomotor activity, food intake, oxygen consumption (VO2), carbon dioxide production (VCO2), energy expenditure (EE) and respiratory exchange ratio (RER), over a period of 3 d. Exercise improved glucose tolerance, VO2, VCO2 and EE in mice fed a HFD (p,0.05). The VO2, VCO2 and EE in AMPKa2 KO HE group were lower than these in WT HE group (p,0.05). Our findings revealed exercise improved glucose tolerance and metabolic disorders in C57 and AMPKa2 KO mice fed a HFD. AMPKa2 is not essential for exercise-induced improvements in glucose tolerance and metabolic disorders.