Watts C, Gain K, Malthus R
Biol Neonate. 1982;41(3-4):204-8. doi: 10.1159/000241550.
The gsd/gsd rat is unable to mobilize liver glycogen due to an absence of phosphorylase b kinase activity. Unlike the normal rat, the maternal gsd/gsd rat cannot maintain its blood glucose concentration in late pregnancy, and values of 3.25 +/- 0.22 mM were found just before birth. The blood glucose of the gsd/gsd fetus falls to 1.76 +/- 0.09 mM at day 19 of gestation and does not rise appreciably again before birth. In contrast, normal fetal rats show a steady rise in blood glucose from hypoglycemic levels at day 19 to a value of 5.70 +/- 0.12 mM on the day of birth. These results indicate that the normal fetal rat contributes towards the regulation of its own glucose in late gestation by utilizing its liver glycogen stores.
由于缺乏磷酸化酶b激酶活性,gsd/gsd大鼠无法动员肝糖原。与正常大鼠不同,gsd/gsd母鼠在妊娠后期无法维持其血糖浓度,在出生前测得的值为3.25±0.22 mM。gsd/gsd胎儿的血糖在妊娠第19天降至1.76±0.09 mM,在出生前没有明显再次升高。相比之下,正常胎儿大鼠的血糖从第19天的低血糖水平稳步上升至出生当天的5.70±0.12 mM。这些结果表明,正常胎儿大鼠在妊娠后期通过利用其肝糖原储备来调节自身的血糖。