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World J Diabetes. Nov 15, 2011; 2(11): 196-203
Published online Nov 15, 2011. doi: 10.4239/wjd.v2.i11.196
Consequences of gestational and pregestational diabetes on placental function and birth weight
Anne Vambergue, Isabelle Fajardy
Anne Vambergue, EA 4489 “Perinatal Environment and Fetal Growth”, Department of Diabetology, Huriez Hospital, 59800 CHRU Lille, France
Isabelle Fajardy, EA 4489 “Perinatal Environment and Fetal Growth”, Biology and Pathology Center, 59800 CHRU Lille, France
Author contributions: Vambergue A and Fajardy I designed and wrote Part I, II, IV, V and part III respectively; all authors approved the final version of the topics (manuscript) to be published.
Correspondence to: Anne Vambergue, Professor, EA 4489 “Perinatal Environment and Fetal Growth”, Department of Diabetology, Huriez Hospital, 59800 CHRU Lille, France. anne.vambergue@chru-lille.fr
Telephone: +33-320-446816 Fax: +33-320-444184
Received: March 18, 2011
Revised: October 19, 2011
Accepted: October 26, 2011
Published online: November 15, 2011
Abstract

Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malformations, materno-fetal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the fetus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The fetoplacental impairment and intrauterine programming of diseases in the offspring’s later life induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence of several developmental and morphological differences in the placenta from rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta from diabetic patients and diabetic experimental models. From both human and rodent diabetic experimental models, it has been suggested that the placenta is a compromised target that largely suffers the impact of maternal diabetes. Depending on the maternal metabolic and proinflammatory derangements, macrosomia is explained by an excessive availability of nutrients and an increase in fetal insulin release, a phenotype related to the programming of glucose intolerance. The degree of fetal damage and placental dysfunction and the availability and utilisation of fetal substrates can lead to the induction of macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multifactorial processes that induce damage to the embryo, the placenta, the fetus and the offspring. Nevertheless, further research is needed to better understand the mechanisms that govern the early embryo development, the induction of congenital anomalies and fetal overgrowth in maternal diabetes.

Keywords: Maternal diabetes; Placental function; Birth weight; Macrosomia; Intrauterine growth retardation