31P-NMR study of the regulation of glycogenolysis in living skeletal muscle.
Based on in vitro biochemical experiments, it is generally believed that glycogenolysis is regulated in two different ways; i.e., Ca2+ regulation at the phosphorylase step and phosphate-product regulation at the phosphofructokinase step. Recent studies on glycogenolysis in living vertebrate skeletal muscles using 31P nuclear magnetic resonance (NMR) presented evidence that glycogenolysis in vivo is regulated by Ca2+ released from the sarcoplasmic reticulum. We performed 31P-NMR studies on living frog skeletal muscle, and found that glycogenolysis is further regulated by the accumulation of phosphate products by contractile activity. Therefore, glycogenolysis in vivo can actually be regulated by the two mechanisms as predicted by in vitro biochemical studies.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006706:Homeostasis; D066298:In Vitro Techniques; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D009119:Muscle Contraction; D009132:Muscles / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D010732:Phosphofructokinase-1 / Q000378:metabolism; D010758:Phosphorus; D006005:Phosphorylases; D011892:Rana catesbeiana
D007461:Iodoacetates; D010758:Phosphorus; D006003:Glycogen; D006005:Phosphorylases; D010732:Phosphofructokinase-1; D002118:Calcium; D019807:Iodoacetic Acid