Loss of hepatic phosphoenolpyruvate carboxykinase 1 dysregulates metabolic responses to acute exercise but enhances adaptations to exercise training in mice
Ferrol I. Rome, Gregory L. Shobert, William C. Voigt, David B. Stagg, Patrycja Puchalska, Shawn C. Burgess, Peter A. Crawford, Curtis C. Hughey
Abstract
Exercise training reduces hepatic steatosis partly through enhanced hepatic terminal oxidation. During acute exercise, hepatic gluconeogenesis is elevated to match the heightened rate of muscle glucose uptake and maintain glucose homeostasis. It has been postulated that the hepatic energetic stress induced by elevating gluconeogenesis during acute exercise is a key stimulus underlying the beneficial metabolic responses to exercise training. This study shows that hepatic gluconeogenesis is not necessary for exercise training to lower liver lipids.
Topics & Concepts
GluconeogenesisSteatosisPhosphoenolpyruvate carboxykinaseInternal medicineEndocrinologyGlucose homeostasisPhysical exerciseAerobic exerciseMedicineMetabolismChemistryInsulinInsulin resistanceBiochemistryEnzymeMetabolism, Diabetes, and CancerLiver Disease Diagnosis and TreatmentAdipose Tissue and Metabolism