| Consequences of gestational and pregestational diabetes on placental function and birth weight. | |
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MedLine Citation:
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PMID: 22087356 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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. |
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Authors:
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Anne Vambergue; Isabelle Fajardy |
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Publication Detail:
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Type: JOURNAL ARTICLE |
Journal Detail:
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Title: World journal of diabetes Volume: 2 ISSN: 1948-9358 ISO Abbreviation: - Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101547524 Medline TA: World J Diabetes Country: - |
Other Details:
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Languages: ENG Pagination: 196-203 Citation Subset: - |
Affiliation:
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Anne Vambergue, EA 4489 "Perinatal Environment and Fetal Growth", Department of Diabetology, Huriez Hospital, 59800 CHRU Lille, France. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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