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

The DOI matches its Crossref record; 147 of the 147 references it cites were found in a registry or an index.

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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Research works printed but not linked: 14

  1. 1995, American Journal of Human Genetics, 57, 160
  2. 1981, Diabetologia, 20, 540
  3. 1989, American Journal of Obstetrics and Gynecology, 160, 1091
  4. 1990, Diabetes/Metabolism Reviews, 16, 147
  5. 1990, Adult offspring from mildly hyperglycemic rats show impairment of glucose regulation and insulin secretion which is transmissible to the next generation, 555
  6. 2008, Diabetologia, 51, 151A
  7. 1997, American Journal of Physiology, 272, E634
  8. 1991, Diabetes, 40, 115
  9. 1996, American Journal of Physiology, 270, E559
  10. 10.1210/en.138.6.2267 · DOI
  11. 2007, American Journal of Physiology—Regulatory Integrative and Comparative Physiology, 292, E187
  12. 10.1172/JCI200421845 · DOI
  13. 2001, American Journal of Physiology—Regulatory Integrative and Comparative Physiology, 281, E592
  14. 2009, Trends in Endocrinology and Metabolism, 21, 223

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Metadata

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 › Endocrinology, Diabetes and Metabolism › 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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