AMPK is indispensable for overload‐induced muscle glucose uptake and glycogenesis but dispensable for inducing hypertrophy in mice

Chronic muscle loading (overload) induces skeletal muscles to undergo hypertrophy and increase glucose uptake. Although AMP-activated protein kinase (AMPK) reportedly serves as a negative regulator of positive uptake, its role in overload-induced uptake is unclear. This study aimed determine whether AMPK regulates muscles. To this end, overload was induced through unilateral synergist ablations wild-type (WT) transgenic mice, expressing the dominant-negative mutation (AMPK-DN). After 14 days, parameters, including fiber cross-sectional area (CSA), glycogen level, vivo [3H]-2-deoxy-D-glucose were assessed. No significant difference observed body weight or blood level between WT AMPK-DN mice. However, 14-day activated pathway mice muscle, whereas response impaired Despite normal CSA gain each type, demonstrated impairment glycogenesis, compared Moreover, changes GLUT4 HKII expression levels reduced that activation indispensable for glycogenesis; however, it dispensable induction Furthermore, AMPK/GLUT4 axes may regulate glycogenesis.