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糖原贮积症大鼠妊娠晚期母鼠和胎鼠的血糖

Blood glucose of mother and fetus late pregnancy of rats with glycogen storage disorder.

作者信息

Watts C, Gain K, Malthus R

出版信息

Biol Neonate. 1982;41(3-4):204-8. doi: 10.1159/000241550.

Abstract

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.

摘要

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。

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