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

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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

DOI 10.1155/2011/105076PMC PMC3202114

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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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Authors: Portha, B., Chavey, A., & Movassat, J.
Affiliations: Centre National de la Recherche Scientifique (FR)
Corresponding author: Portha, Bernard
ORCID: Movassat, Jamileh
Venue: Experimental Diabetes Research
Publisher: Wiley
Published: 2011
Volume: 2011
Pages: 1-16
ISSN: 1687-5214 (ISSN-L)
1687-5303
DOI: 10.1155/2011/105076
PMC: PMC3202114
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: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (unspecified)
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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Early-Life Origins of Type 2 Diabetes: Fetal Programming of the Beta-Cell Mass

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