Maternal Lipids and Fetal Overgrowth: Making Fat from Fat.

Maternal Lipids and Fetal Overgrowth: Making Fat from Fat.
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DOI:
10.1016/j.clinthera.2018.08.007
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发表时间:
2018-10
影响因子:
3.2
通讯作者:
Hernandez TL
Hernandez TL
中科院分区:
医学3区
文献类型:
--
作者:
Barbour LA;Hernandez TL

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越来越多的人认识到,母体葡萄糖浓度低于以前用于诊断妊娠期糖尿病(GDM)和治疗目标的浓度可能导致胎儿过度生长。然而,患有GDM的母亲似乎具有最佳的血糖控制,肥胖和正常葡萄糖耐量的母亲仍然具有显著增加的分娩大于胎龄(LGA)婴儿的风险,或者更重要的是,出生时肥胖增加。不太了解的是,除了葡萄糖之外,母体脂质也是胎儿脂肪堆积的底物,胎盘脂肪酶可以将母体甘油三酯(TG)水解为游离脂肪酸(FFA),以供胎儿-胎盘利用。与正常体重(NW)的母亲相比,肥胖和GDM的母亲在怀孕早期的母亲TG平均高出40-50%,并且在整个怀孕期间维持在较高水平。越来越多的证据支持母亲的TG,包括空腹(FTG)和餐后(PPTG),也是新生儿肥胖(新生儿%脂肪)的预测因子,这是儿童肥胖的一个危险因素,并且早期暴露至少与肥胖母亲的晚期暴露一样强。在母体营养过剩和母体胰岛素抵抗(导致胎儿高胰岛素血症)的情况下,胎儿过量的FFA暴露可能导致皮下和其他部位的脂质蓄积和胎儿脂肪发育。在这篇评论中,我们提供了进一步的证据,以证明在妊娠早期TG升高的肥胖母亲中靶向母体FTG和PPTG,以确定降低TG的干预方法是否可能限制胎儿过度生长,并可能减轻宫内对儿童肥胖和代谢疾病的贡献。
There is an increasing recognition that maternal glucose concentrations lower than those previously used to diagnosis gestational diabetes mellitus (GDM) and target for treatment can result in excess fetal growth. Yet, mothers with GDM who appear to have optimal glycemic control and mothers with obesity and normal glucose tolerance still have a significantly increased risk for delivering infants who are large-for-gestational-age (LGA), or even more importantly, who have increased adiposity at birth. What is less appreciated is that in addition to glucose, maternal lipids are also substrates for fetal fat accretion and that placental lipases can hydrolyze maternal triglycerides (TG) to free fatty acids (FFA) for fetal-placental availability. Maternal TG are 40–50% higher on average in mothers with obesity and GDM compared to normal-weight (NW) mothers early in pregnancy and are sustained at a higher level throughout gestation. Increasing evidence supports that maternal TG, both fasting (FTG) and postprandial (PPTG), are also predictors of newborn adiposity (newborn %fat), a risk factor for childhood obesity, and that early exposure is at least as strong of a risk factor as later exposure in mothers with obesity. In the setting of maternal nutrient excess and maternal insulin resistance, which lead to fetal hyperinsulinemia, excess FFA exposure to the fetus may result in lipid storage and fetal fat development in subcutaneous and possibly other depots. In this commentary, we provide further evidence to make a case for targeting maternal FTG and PPTG in mothers with obesity who have elevated TG in early pregnancy to determine whether a TG-lowering interventional approach might limit fetal overgrowth and potentially mitigate the intrauterine contribution towards childhood obesity and metabolic disease.
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