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Prenatal Programming of Insulin Secretion in Intrauterine Growth Restriction

GATFORD, KATHRYN L. PhD*; SIMMONS, REBECCA A. MD

Clinical Obstetrics and Gynecology: September 2013 - Volume 56 - Issue 3 - p 520–528
doi: 10.1097/GRF.0b013e31829e5b29
Fetal Origins of Adult Disease

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.

*Robinson Institute, and School of Paediatrics and Reproductive Health, University of Adelaide, SA, Australia;

Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

The authors declare that they have nothing to disclose.

Correspondence: Kathryn L. Gatford, PhD, School of Paediatrics and Reproductive Health, Faculty of Health Sciences, The University of Adelaide, Room 620F, 6th Floor Medical School North, SA, Australia. E-mail: kathy.gatford@adelaide.edu.au

© 2013 by Lippincott Williams & Wilkins.