Epigenetic mechanisms in the development of type 2 diabetes

Pinney, Sara E.; Simmons, Rebecca A.

doi:10.1016/j.tem.2009.10.002

Cited by 205Birth, Development, and HealthEpigenetics and DNA MethylationPancreatic function and diabetes

Epigenetic mechanisms in the development of type 2 diabetes

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Pinney, Sara E., Simmons, Rebecca A.·2010·Trends in Endocrinology & Metabolism

DOI 10.1016/j.tem.2009.10.002PMC PMC2848901

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Abstract

Type 2 diabetes (T2D) is a disorder of complex genetics influenced by interactions between susceptible genetic loci and environmental perturbations. Intrauterine growth retardation is one such environmental perturbation linked to the development of T2D in adulthood. An abnormal metabolic intrauterine milieu affects fetal development by permanently modifying expression of key genes regulating beta-cell development (Pdx1) and glucose transport (Glut4) in muscle. Epigenetic regulation of gene expression is one mechanism by which genetic susceptibility and environmental insults can lead to T2D. Therefore, therapeutic agents targeting epigenetic gene regulation can ultimately be used to treat T2D; however, there is much to be learned about genome-wide epigenetic programming of health and disease before these therapies can be used in patient care.

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Loss of β-cell mass in growth-restricted rats has been linked to epigenetic downregulation of Pdx1, which is essential for normal β-cell differentiation.
“This loss of β-cell mass has been linked to epigenetic downregulation of pancreatic homeobox transcription factor (Pdx1), which is essential for normal β-cell differentiation in the embryo [79].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [79]
The ‘Chromatin Remodeling in the β-cell of IUGR rats’ section reports epigenetic repression of Pdx-1 in growth-restricted rats and describes its critical role in pancreatic development and β-cell differentiation. It does not link that repression to a loss of β-cell mass; it instead discusses β-cell secretory dysfunction, and notes that a milder Pdx-1 reduction in mice permits normal β-cell mass. Page numbers were not available in our copy. (LLM, conf=0.87)
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Vaiserman, A. M., & Lushchak, O. V. (2019) · International Journal of Genomics · doi:10.1155/2019/3821409 · Cited by 34 · see citing works
Developmental Origins of β-Cell Failure in Type 2 Diabetes: The Role of Epigenetic Mechanisms
Simmons, R. A. (2007) · Pediatric Research · doi:10.1203/pdr.0b013e3180457623 · Cited by 67 · see citing works
Self-citation

Authors: Pinney, S. E., & Simmons, R. A.
Affiliations: Children's Hospital of Philadelphia (US)
ORCID: Pinney, Sara E.
Simmons, Rebecca A.
Venue: Trends in Endocrinology & Metabolism
Publisher: Elsevier BV
Published: 2010-04
Volume: 21
Issue: 4
Pages: 223-229
ISSN: 1043-2760 (ISSN-L)
DOI: 10.1016/j.tem.2009.10.002
PMC: PMC2848901
OpenAlex: W1977200537
Cited by: 205
References: 66
Citations by year: 2026: 6 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 8 · 2021: 9 · 2020: 8 · 2019: 7 · 2018: 11 · 2017: 13 · 2016: 14 · 2015: 17 · 2014: 22 · 2013: 27 · 2012: 19
FWCI: 2.30
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Endocrinology and Metabolism (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute on Aging (R01AG020898)
National Institute of Diabetes and Digestive and Kidney Diseases (L40 DK079770, R01DK055704, DK-55704)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD0432545)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords: type 2 diabetes, epigenetic regulation, fetal growth restriction, fetal programming, beta-cell development, PDX1, GLUT4, gene-environment interaction, epigenetic therapy, gene expression
MeSH terms: Diabetes Mellitus, Type 2, Fetal Growth Retardation, Gene Expression Regulation, Histones, Humans, Trans-Activators, Oxidative Stress, Homeodomain Proteins, Chromatin Assembly and Disassembly, Epigenesis, Genetic, Glucose Transporter Type 4

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Epigenetic mechanisms in the development of type 2 diabetes

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