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Placental control of metabolic adaptations in the mother for an optimal pregnancy outcome. What goes wrong in gestational diabetes?

Abstract：

:As pregnancy progresses the placental syncytiotrophoblast increasingly assumes control of maternal glucose homeostasis through the release and counter-balancing effects of placental lactogen (PL) and placental variant growth hormone (GH-V). While local actions of these hormones on placental growth and function are likely to exist, each also exerts indirect actions to ensure fetal nutritional availability through modulation of the maternal insulin/insulin-like growth factor axis. Peripheral insulin resistance results from the increasing levels of GH-V in the maternal circulation and is counter-balanced by an increase in insulin availability through an expansion of maternal pancreatic β-cell mass. GH-V also increases maternal IGF-1 synthesis leading to enhanced placental growth and nutrient transporter activity. Maternal obesity and the presence of diabetes in pregnancy is associated with a disrupted balance in the placental expression of PL and GH-V. Several parallel mechanisms are likely to contribute to the increasing maternal β-cell mass as gestation progresses, including a reactivation of β-cell proliferation, an expansion of subsequent differentiation of resident β-cell progenitors, and α-to β-cell trans-differentiation. Each of these pathways could potentially be modulated during pregnancy to increase β-cell mass and prevent the onset of gestational diabetes.

journal_name

Placenta

journal_title

Placenta

authors

Hill DJ

doi

10.1016/j.placenta.2018.01.002

subject

Has Abstract

pub_date

2018-09-01 00:00:00

pages

162-168

eissn

0143-4004

issn

1532-3102

pii

S0143-4004(18)30004-3

journal_volume

69

pub_type

杂志文章,评审

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