Affiliation:
1. Lawson Health Research Institute, St. Joseph’s Health Care, 268 Grosvenor Street, London, Ontario N6A 4V2, Canada
Abstract
Normal pregnancy is associated with increased insulin resistance as a metabolic adaptation to
the nutritional demands of the placenta and fetus, and this is amplified in obese mothers. Insulin resistance
is normally compensated for by an adaptive increase in pancreatic β-cell mass together with enhanced
glucose-stimulated insulin release. Placentally-derived hormones and growth factors are central
to the altered pancreatic morphology and function. A failure of β-cells to undergo adaptive change after
the first trimester has been linked with gestational diabetes. In the pregnant mouse, an increase in β-cell
replication contributes to a 2-3-fold increase in mass peaking in late gestation, depending on the proliferation
of existing β-cells, the differentiation of resident progenitor β-cells, or islet cell transdifferentiation.
Using mouse models and human studies placenta- and islet of Langerhans-derived molecules
have been identified that are likely to contribute to the metabolic adaptations to pregnancy and
whose physiology is altered in the obese, glucose-intolerant mother. Maternal obesity during pregnancy
can create a pro-inflammatory environment that can disrupt the response of the β-cells to the endocrine
signals of pregnancy and limit the adaptive changes in β-cell mass and function, resulting in an increased
risk of gestational diabetes.
Funder
Canadian Institutes of Health Research
Publisher
Bentham Science Publishers Ltd.
Subject
Cardiology and Cardiovascular Medicine,Pharmacology
Cited by
20 articles.
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