胎儿
高胰岛素血症
内分泌学
巨大儿
内科学
血糖性
胎盘
医学
胎盘功能不全
妊娠期糖尿病
妊娠期
胰岛素
怀孕
生物
胰岛素抵抗
遗传学
作者
C M Macfarlane,N. Tsakalakos
出处
期刊:PubMed
[National Institutes of Health]
日期:1988-01-01
卷期号:6 (2): 68-73
被引量:24
摘要
The Pedersen hypothesis of fetal macrosomia in neonates born to diabetic mothers has been extended. In neonates born to gestational diabetic mothers, it is suggested that an intrinsic fetal pancreatic beta-cell hyperplasia 'pulls' glucose across the placenta, i.e. assists in glycemic control of the mother. The initial increase in fetal size due to fetal hyperinsulinism gives rise to developing hypoxemia, and the limitation in fetal oxygen availability alters differential tissue utilization of glucose, increases alpha-glycerophosphate synthesis in fetal adipocytes, and gives rise to a further increase in fetal adiposity.
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