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Cited by 299Birth, Development, and HealthGestational Diabetes Research and ManagementPancreatic function and diabetes

Consequences of Fetal Exposure to Maternal Diabetes in Offspring

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Fetita, Lila-Sabrina, Sobngwi, Eugène, Serradas, Patricia, Calvo, Fabien, Gautier, Jean-François·2006·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jc.2006-0624
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Abstract

CONTEXT: 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. EVIDENCE ACQUISITION: A MEDLINE search covered the period from 1960-2005. EVIDENCE SYNTHESIS: 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. CONCLUSION: 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.

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  • Excess fetal insulin production can stress developing pancreatic β-cells, contributing to β-cell dysfunction and insulin resistance prenatally.

    “As previously mentioned, excess fetal insulin production can stress the developing pancreatic β-cells, contributing to β-cell dysfunction and insulin resistance, even prenatally [62].”

    From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [62]

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Authors
Fetita, L.-S., Sobngwi, E., Serradas, P., Calvo, F., & Gautier, J.-F.
Affiliations
  • Inserm (FR)
  • Assistance Publique-Hopitaux de Paris (L.-S.F., E.S., J.-F.G.), Department of Endocrinology and Diabetes, Saint-Louis Hospital, University Paris 7, 75475 Paris Cedex 10, France
  • Centre National de la Recherche Scientifique (FR)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2006-10-01
Volume
91
Issue
10
Pages
3718-3724
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jc.2006-0624
OpenAlex
W2101063948
Cited by
299
References
105
Citations by year
2026: 4 · 2025: 5 · 2024: 15 · 2023: 15 · 2022: 28 · 2021: 21 · 2020: 12 · 2019: 15 · 2018: 17 · 2017: 17 · 2016: 16 · 2015: 15 · 2014: 16 · 2013: 15 · 2012: 10
FWCI
1.75
Type
journal article
Language
en
Open access
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Newcastle University ePrints (Newcastle Univesity)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
maternal diabetes, prenatal exposure, type 2 diabetes, impaired glucose tolerance, insulin resistance, insulin secretion defect, epigenetic inheritance, beta-cell dysfunction, pancreatic innervation, genomic imprinting, intrauterine hyperglycemia, glycemic control in pregnancy, diabetes epidemic
MeSH terms
Adult, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Female, Fetus, Homeostasis, Humans, Insulin Resistance, Pancreas, Pregnancy, Diabetes, Gestational, Neovascularization, Physiologic

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