Simulation study of control of hepatic glycogen synthesis by glucose and insulin.
The plausibility of various hypotheses concerning the effects of glucow dynamic model of glucose metabolism in the liver. The model consisted of six compartments representing extracellular glucose, and intracellular glucose, glucose 6-phosphate, glucose 1-phosphate, uridine diphosphate glucose, obtained from literature reports, the model predicted values of intermediates which were close to those reported for the liver, sampled from fasting animals. The model predicts that glucose can generate significant glycogen deposition by engendering the inhibition of glucose-6-phosphatase, but not by mass action, glycogen synthase activation, or phosphorylase deactivation. The model predicts that, although insulin can inhibit glucose production by lowering phosphorylase and gluconeogenesis, only an insulin-mediated induction of glucokinase can account for insulin's action to potentiate the effect of glucose alone on glycogen synthesis.
D005947:Glucose / Q000494:pharmacology*; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D008099:Liver / Q000201:enzymology; D008112:Liver Glycogen / Q000096:biosynthesis*; D008954:Models, Biological; D006005:Phosphorylases / Q000378:metabolism
D007328:Insulin; D008112:Liver Glycogen; D006005:Phosphorylases; D006006:Glycogen Synthase; D005952:Glucose-6-Phosphatase; D005947:Glucose