Cited by 127Birth, Development, and HealthPancreatic function and diabetesGestational Diabetes Research and Management

Early-Life Origins of Type 2 Diabetes: Fetal Programming of the Beta-Cell Mass

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Portha, Bernard, Chavey, Audrey, Movassat, Jamileh·2011·Experimental Diabetes Research

Abstract

A substantial body of evidence suggests that an abnormal intrauterine milieu elicited by maternal metabolic disturbances as diverse as undernutrition, placental insufficiency, diabetes or obesity, may program susceptibility in the fetus to later develop chronic degenerative diseases, such as obesity, hypertension, cardiovascular diseases and diabetes. This paper examines the developmental programming of glucose intolerance/diabetes by disturbed intrauterine metabolic condition experimentally obtained in various rodent models of maternal protein restriction, caloric restriction, overnutrition or diabetes, with a focus on the alteration of the developing beta-cell mass. In most of the cases, whatever the type of initial maternal metabolic stress, the beta-cell adaptive growth which normally occurs during gestation, does not take place in the pregnant offspring and this results in the development of gestational diabetes. Therefore gestational diabetes turns to be the ultimate insult targeting the offspring beta-cell mass and propagates diabetes risk to the next generation again. The aetiology and the transmission of spontaneous diabetes as encountered in the GK/Par rat model of type 2 diabetes, are discussed in such a perspective. This review also discusses the non-genomic mechanisms involved in the installation of the programmed effect as well as in its intergenerational transmission.

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Crossref · 10.1155/2011/105076

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  • Individuals who experienced overnutrition in the womb are more likely to have experienced hyperglycemia and β-cell fatigue before birth, predisposing them to hyperglycemia during later metabolic stress such as pregnancy.

    “These individuals are more likely to have experienced hyperglycemia and β-cell fatigue even before birth, predisposing them to hyperglycemia during times of later metabolic stress, such as during pregnancy [55].”

    From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [55]

    Section 4 (page unavailable) links early-life stressors, including maternal overnutrition, to later endocrine pancreatic deficiency and says pregnancy can expose a latent low insulin response in female offspring. It also describes hyperglycemia during fetal and/or early postnatal life. The copy does not establish that overnourished individuals experienced β-cell fatigue before birth; the discussion relies substantially on animal models and does not isolate prenatal exposure for every case. (LLM, conf=0.84)

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Authors
Portha, B., Chavey, A., & Movassat, J.
Affiliations
Centre National de la Recherche Scientifique (FR)
Corresponding author
Portha, Bernard
Venue
Experimental Diabetes Research
Publisher
Wiley
Published
2011
Volume
2011
Pages
1-16
ISSN
  • 1687-5214 (ISSN-L)
  • 1687-5303
OpenAlex
W2154337610
Cited by
127
References
147
Citations by year
2026: 4 · 2025: 5 · 2024: 3 · 2023: 4 · 2022: 7 · 2021: 7 · 2020: 10 · 2019: 7 · 2018: 6 · 2017: 10 · 2016: 15 · 2015: 11 · 2014: 13 · 2013: 11 · 2012: 14
FWCI
1.82
Type
journal article
Language
en
Open access
Locations
  • Experimental Diabetes Research (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • French National Research Agency (ANR-06-PHYSIO-028)
  • Égide (ANR-06-PHYSIO-028)
  • NEB Association (ANR-06-PHYSIO-028)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
type 2 diabetes, fetal programming, beta-cell mass, maternal protein restriction, caloric restriction, maternal overnutrition, maternal diabetes, gestational diabetes mellitus, impaired glucose tolerance, intergenerational transmission, developmental programming
MeSH terms
Animals, Energy Intake, Diabetes Mellitus, Type 2, Disease Models, Animal, Female, Humans, Male, Pancreas, Pregnancy, Pregnancy in Diabetics, Prenatal Exposure Delayed Effects, Protein Deficiency, Risk Factors, Diabetes, Gestational, Overnutrition, Fetal Development, Insulin-Secreting Cells, Mice, Rats

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