Prenatal programming of insulin secretion in intrauterine growth restriction.

Abstract:

:Intrauterine growth restriction (IUGR) impairs insulin secretion in humans and in animal models of IUGR. Several underlying mechanisms have been implicated, including decreased expression of molecular regulators of β-cell mass and function, in some cases shown to be due to epigenetic changes initiated by an adverse fetal environment. Alterations in cell cycle progression contribute to loss of β-cell mass, whereas decreased islet vascularity and mitochondrial dysfunction impair β-cell function in IUGR rodents. Animal models of IUGR sharing similar insulin secretion outcomes as the IUGR human are allowing underlying mechanisms to be identified. This review will focus on models of uteroplacental insufficiency.

journal_name

Clin Obstet Gynecol

authors

Gatford KL,Simmons RA

doi

10.1097/GRF.0b013e31829e5b29

subject

Has Abstract

pub_date

2013-09-01 00:00:00

pages

520-8

issue

3

eissn

0009-9201

issn

1532-5520

journal_volume

56

pub_type

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