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正常和糖尿病大鼠在器官发生早期,母体低血糖会损害胚胎发育。

Embryonic growth impaired by maternal hypoglycemia during early organogenesis in normal and diabetic rats.

作者信息

Kawaguchi M, Tanigawa K, Tanaka O, Kato Y

机构信息

Department of Internal Medicine, Shimane Medical University, Izumo, Japan.

出版信息

Acta Diabetol. 1994 Sep;31(3):141-6. doi: 10.1007/BF00570368.

Abstract

The effect of maternal hypoglycemia on early organogenesis was studied in normal and diabetic rats. Female Wistar rats were made diabetic by an intravenous injection of streptozotocin (45 mg/kg) 2-3 weeks before conception. On day 9.5 or 10.5 of embryo development, both control and diabetic dams received saline or Actrapid human insulin (400 mU/rat) intraperitoneally after 19-h starvation. The fasting plasma glucose levels in diabetic dams decreased from approximately 23 to 8 mM. Hypoglycemia as low as 3.5 mM was maintained for 60 min in insulin-treated mother rats. Pregnancy was terminated on day 11.6 of embryo development. A significant growth retardation was found in diabetic embryos as compared with normal embryos. Maternal hypoglycemia lowered the DNA content in normal but not diabetic embryos, while the teratogenic effect of maternal hypoglycemia was not pronounced in either normal or diabetic embryos. These data may suggest that maternal hypoglycemia in vivo in early pregnancy influences the embryogenesis but not teratogenesis of rat embryos.

摘要

在正常和糖尿病大鼠中研究了母体低血糖对早期器官发生的影响。在受孕前2 - 3周,通过静脉注射链脲佐菌素(45毫克/千克)使雌性Wistar大鼠患糖尿病。在胚胎发育的第9.5天或10.5天,对照组和糖尿病母鼠在禁食19小时后腹腔注射生理盐水或Actrapid人胰岛素(400 mU/只)。糖尿病母鼠的空腹血糖水平从约23毫摩尔/升降至8毫摩尔/升。胰岛素治疗的母鼠中,低血糖水平低至3.5毫摩尔/升并维持60分钟。在胚胎发育的第11.6天终止妊娠。与正常胚胎相比,糖尿病胚胎出现显著的生长迟缓。母体低血糖降低了正常胚胎而非糖尿病胚胎中的DNA含量,而母体低血糖的致畸作用在正常或糖尿病胚胎中均不明显。这些数据可能表明,妊娠早期母体体内的低血糖会影响大鼠胚胎的胚胎发生,但不会影响其致畸作用。

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