title: Consequences of fetal exposure to maternal diabetes in offspring.
abstract: BACKGROUND
  Type 2 diabetes is the result of both genetic and environmental factors. Fetal exposure to maternal diabetes is associated with a higher risk of abnormal glucose homeostasis in offspring beyond that attributable to genetic factors, and therefore, may participate in the excess of maternal transmission of type 2 diabetes.
  
  
  METHODS
  A MEDLINE search covered the period from 1960-2005.
  
  
  RESULTS
  Human studies performed in children and adolescents suggest that offspring who had been exposed to maternal diabetes during fetal life exhibit higher prevalence of impaired glucose tolerance and markers of insulin resistance. Recent studies that directly measured insulin sensitivity and insulin secretion have shown an insulin secretory defect even in the absence of impaired glucose tolerance in adult offspring. In animal models, exposure to a hyperglycemic intrauterine environment also led to the impairment of glucose tolerance in the adult offspring. These metabolic abnormalities were transmitted to the next generations, suggesting that in utero exposure to maternal diabetes has an epigenetic impact. At the cellular level, some findings suggest an impaired pancreatic beta-cell mass and function. Several mechanisms such as defects in pancreatic angiogenesis and innervation, or modification of parental imprinting, may be implicated, acting either independently or in combination.
  
  
  CONCLUSIONS
  Thus, fetal exposure to maternal diabetes may contribute to the worldwide diabetes epidemic. Public health interventions targeting high-risk populations should focus on long-term follow-up of subjects who have been exposed in utero to a diabetic environment and on a better glycemic control during pregnancy.
authors.affiliation: Department of Endocrinology and Diabetes, Saint-Louis Hospital, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France.
authors.forename: Lila-Sabrina
authors.initials: LS
authors.lastname: Fetita
authors.forename: Eugène
authors.initials: E
authors.lastname: Sobngwi
authors.forename: Patricia
authors.initials: P
authors.lastname: Serradas
authors.forename: Fabien
authors.initials: F
authors.lastname: Calvo
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Gautier
mesh_terms: D000328:Adult; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism*; D016640:Diabetes, Gestational / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005333:Fetus / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance; D018919:Neovascularization, Physiologic; D010179:Pancreas / Q000098:blood supply / Q000294:innervation; D011247:Pregnancy
chemical_list: D001786:Blood Glucose