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
Open accessAbstract
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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“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]
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Cites
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Flagged first, then by citations
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Cited by
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The Pathophysiology of Gestational Diabetes Mellitus
Plows, J. F., Stanley, J. L., Baker, P. N., Reynolds, C. M., & Vickers, M. H. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19113342 · Cited by 1,874
“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].”
BackgroundDifferentiation of diabetes by pathophysiology, natural history, and prognosis
Skyler, J. S., Bakris, G. L., Bonifacio, E., Darsow, T., Eckel, R. H., Groop, L., Groop, P.-H., Handelsman, Y., Insel, R. A., Mathieu, C., et al. (2017) · Diabetes · doi:10.2337/db16-0806 · Cited by 823
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Gut microbiota, immune development and function
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Pathogenesis of MASLD and MASH – role of insulin resistance and lipotoxicity
Bansal, S., & Bansal, M. B. (2024) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.17930 · Cited by 211
Metadata
- 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
- 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
- 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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