[The regulation of glycogen synthesis in the fetal rat liver in the near term].
In order to clarify the mechanism of regulation of glycogen metabolism in fetal rat liver during gestation, we measured glycogen synthetase activity, and the binding capacity of the insulin receptor. We also examined the possibility of glycogen synthesis through gluconeogenesis. Major findings are as follows: 1) Glycogen content in fetal liver increased dramatically during gestation and peaked on Day 21 of gestation (one day before delivery). 2) Both the total glycogen synthetase activity (a: active enzyme+b: inactive enzyme) and the ratio of the activities of a to a+b also rose during gestation, suggesting that an increase in the active form of glycogen synthetase is a major cause of the increase in the amount of glycogen in fetal liver. 3) Insulin is known to stimulate glycogen synthesis by activating glycogen synthetase. However, the number and the affinity constant of the insulin receptor in fetal liver did not changed, although the concentration of serum insulin increased during gestation. 4) The ratio of glycogen synthesized from serum glycerol relative to that from serum glucose plus glycerol increased from 8% on Day 19 to 22% on Day 21. Since stimulation of gluconeogenesis is considered to result in an accumulation of glucose-6-phosphate, a potent activator for glycogen synthetase, glyconeogenesis from glycerol may play an important role in glycogen storage in fetal liver.
Ienaga
S
S
Department of Obstetrics and Gynecology, Nippon Medical School Hospital, Tokyo, Japan.
D000818:Animals; D005260:Female; D005333:Fetus / Q000378:metabolism*; D006003:Glycogen / Q000096:biosynthesis*; D006006:Glycogen Synthase / Q000378:metabolism / Q000502:physiology; D006706:Homeostasis; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D011972:Receptor, Insulin / Q000378:metabolism
D007328:Insulin; D006003:Glycogen; D006006:Glycogen Synthase; D011972:Receptor, Insulin