Gain K R, Watts C
Biol Neonate. 1986;49(3):140-9. doi: 10.1159/000242524.
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.
对同时含有杂合子和纯合子gsd/gsd大鼠的窝仔进行了研究,以确定胎儿肝脏糖原是否有助于胎儿血糖池。结果表明,在所有研究的年龄段,纯合子gsd/gsd胎儿(无法动员肝脏糖原)的血糖浓度始终低于其杂合子(正常)同窝仔。这种差异与母体类型和母体血糖浓度无关。在妊娠21天时,杂合子胎儿的肝脏磷酸化酶有明显激活,同时胎儿/母体血糖比值显著升高。相比之下,纯合同窝仔的磷酸化酶没有明显激活,比值也没有升高。在纯合子胎儿中,血糖浓度保持较低,肝脏糖原含量较高。文中讨论了胎儿肝脏糖原来源于糖异生前体的可能性。