Relationship between liver glycogen metabolism and glucose homeostasis in the fetal rat: studies with the gsd/gsd rat.
Litters containing both heterozygous and homozygous gsd/gsd rats have been studied to determine whether fetal liver glycogen contributes to the fetal blood glucose pool. It is shown that homozygous gsd/gsd fetuses (unable to mobilise liver glycogen) have consistently lower blood glucose concentrations than their heterozygous (normal) littermates at all ages studied. This difference is independent of maternal type and maternal blood glucose concentration. There is a marked activation of liver phosphorylase in heterozygous fetuses at 21 days of gestation, associated with a significant rise in the fetal/maternal blood glucose ratio. In contrast, there is no significant activation of phosphorylase or rise in the ratio for homozygous littermates. In homozygous fetuses, the blood glucose concentrations remained low and liver glycogen high. The possibility of fetal liver glycogen being derived from gluconeogenic precursors is discussed.
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D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005865:Gestational Age; D006003:Glycogen / Q000378:metabolism*; D006008:Glycogen Storage Disease / Q000235:genetics / Q000378:metabolism*; D006579:Heterozygote; D006706:Homeostasis; D006720:Homozygote; D008099:Liver / Q000196:embryology* / Q000378:metabolism; D010764:Phosphorylase Kinase / Q000172:deficiency; D010762:Phosphorylase a / Q000378:metabolism; D011247:Pregnancy; D051381:Rats
D001786:Blood Glucose; D006003:Glycogen; D010762:Phosphorylase a; D010764:Phosphorylase Kinase