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The cellular energy sensor AMP-activated protein kinase (AMPK) is a metabolicregulator that mediates adaptation to nutritional variations in order tomaintain a proper energy balance in cells. We show here that suckling-weaningand fasting-refeeding transitions in rodents are associated with changes inAMPK activation and the cellular energy state in the liver. These nutritionaltransitions were characterized by a metabolic switch from lipid to glucoseutilization, orchestrated by modifications in glucose levels and theglucagon:insulin ratio in the bloodstream. We therefore investigated therespective roles of glucose and pancreatic hormones on AMPK activation in mouseprimary hepatocytes. We found that glucose starvation transiently activatesAMPK, whereas changes in glucagon and insulin levels had no impact on AMPK.Challenge of hepatocytes with metformin-induced metabolic stress strengthenedboth AMPK activation and cellular energy depletion limited-glucose conditions,whereas neither glucagon nor insulin altered AMPK activation. Although bothinsulin and glucagon induced AMPK$\alpha$ phosphorylation at its Ser-485/491residue, they did not affect its activity. Finally, the decrease in cellularATP levels in response to an energy stress was additionally exacerbated underfasting conditions and by AMPK deficiency in hepatocytes, revealing metabolicinflexibility and emphasizing the importance of AMPK for maintaining hepaticenergy charge. Our results suggest that nutritional changes (i.e. glucoseavailability), rather than the related hormonal changes (i.e. theglucagon:insulin ratio), sensitize AMPK activation to the energetic stressinduced by the dietary transition during fasting. This effect is critical forpreserving the cellular energy state in the liver.

Glucose availability but not changes in pancreatic hormones sensitizes hepatic AMPK activity during nutritional transition in rodents