31P NMR study of the regulation of glycogenolysis in iodoacetate-treated skeletal muscle.
Extensive in vitro biochemical experiments have established that glycogenolysis is regulated in two different ways; i.e., the Ca regulation at the phosphorylase step and the phosphate-product regulation at the phosphofructokinase step. Recent studies on glycogenolysis in living vertebrate skeletal muscles by use of 31P nuclear magnetic resonance (NMR) presented evidence that glycogenolysis in vivo is regulated by the Ca released from the sarcoplasmic reticulum (SR) but not by the phosphate products. We have performed 31P NMR studies on living frog skeletal muscle, and have shown that glycogenolysis is regulated not only by the Ca from the SR but also by the accumulation of phosphate products by contraction. This indicates that the glycogenolysis in vivo can be actually regulated by the two mechanisms as predicted by in vitro biochemical studies.
Yamada
T
T
Department of Physiology, School of Medicine, Teikyo University, Tokyo, Japan.
Sugi
H
H
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006003:Glycogen / Q000378:metabolism*; 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*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus; D011898:Ranidae
D007461:Iodoacetates; D010710:Phosphates; D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate; D006003:Glycogen; D019807:Iodoacetic Acid