Exercise training adaptations in liver glycogen and glycerolipids require hepatic AMP-activated protein kinase in mice
Curtis C. Hughey, Deanna P. Bracy, Ferrol I. Rome, Mickael Goelzer, E. Patrick Donahue, Benoı̂t Viollet, Marc Foretz, David H. Wasserman
Abstract
This study shows that the energy sensor and transducer, AMP-activated protein kinase (AMPK), is necessary for an exercise training-induced: 1) increase in liver glycogen that is necessary for accelerated glycogenolysis during exercise, 2) decrease in liver glycerolipids independent of tricarboxylic acid (TCA) cycle flux, and 3) decline in the desaturation and elongation of fatty acids comprising liver diacylglycerides. The mechanisms defined in these studies have implications for use of regular exercise or AMPK-activators in patients with fatty liver.
Topics & Concepts
AMPKGlycogenolysisGlycogenGluconeogenesisInternal medicineEndocrinologyAMP-activated protein kinaseProtein kinase ALipid metabolismFatty liverMetabolismChemistryBiologyKinaseMedicineBiochemistryDiseaseMetabolism, Diabetes, and CancerPancreatic function and diabetesAdipose Tissue and Metabolism