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[母体高血糖对胎儿生长机制的影响]

[Effects of maternal hyperglycemia on fetal growing mechanism].

作者信息

Kobayashi A, Ueda Y, Morikawa H, Mochizuki M

机构信息

Department of Obstetrics and Gynecology, Kobe University School of Medicine.

出版信息

Nihon Sanka Fujinka Gakkai Zasshi. 1991 Mar;43(3):289-96.

PMID:1828480
Abstract

The aim of this study was to clarify the effects of maternal hyperglycemia on fetal growth in rats. In streptozotocin (STZ)-induced diabetic rats, maternal serum glucose levels during pregnancy were controlled by daily injection of NPH insulin or saline from day 3 to 21 of pregnancy. The body weight, hepatic glycogen content and serum concentrations of insulin and Insulin-like Growth Factor-I (IGF-I) in fetuses from these rats were measured on Day 21 of pregnancy. Fetal body weight positively correlated with maternal mean blood glucose (MBG) during pregnancy in the groups of diabetic mothers whose MBG was less than 220 mg/dl, whereas a negative correlation was observed in the groups whose MBG was more than 220 mg/dl. In addition, a similar correlation between hepatic glycogen content, serum concentrations of insulin or IGF-I and maternal MBG was observed. On the other hand, in the culture of fetal rat hepatocytes, glycogen content indicated a dose-related increase according to the increase in glucose concentration in the medium. These results suggest that the growth retardation observed in rats whose maternal mean glucose level is higher than 220 mg/dl is not caused by abnormalities in the metabolic function of the fetal metabolic organ (liver), but it is caused by a decrease in the production and/or secretion of growth-promoting factors (for example insulin and IGF-I) in the fetuses.

摘要

本研究的目的是阐明母体高血糖对大鼠胎儿生长的影响。在链脲佐菌素(STZ)诱导的糖尿病大鼠中,从妊娠第3天至21天,通过每日注射中性鱼精蛋白锌胰岛素或生理盐水来控制孕期母体血清葡萄糖水平。在妊娠第21天测量这些大鼠胎儿的体重、肝糖原含量以及胰岛素和胰岛素样生长因子-I(IGF-I)的血清浓度。在母体平均血糖(MBG)低于220mg/dl的糖尿病母亲组中,胎儿体重与孕期母体平均血糖呈正相关,而在MBG高于220mg/dl的组中观察到负相关。此外,在肝糖原含量、胰岛素或IGF-I血清浓度与母体MBG之间也观察到类似的相关性。另一方面,在胎鼠肝细胞培养中,糖原含量随着培养基中葡萄糖浓度的增加呈剂量相关增加。这些结果表明,母体平均葡萄糖水平高于220mg/dl的大鼠中观察到的生长迟缓不是由胎儿代谢器官(肝脏)代谢功能异常引起的,而是由胎儿中生长促进因子(例如胰岛素和IGF-I)的产生和/或分泌减少引起的。

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