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Epigenetic mechanisms in the development of type 2 diabetes
Open accessAbstract
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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“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]
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Self-citation
Metadata
- Authors
- Pinney, S. E., & Simmons, R. A.
- Affiliations
- Children's Hospital of Philadelphia (US)
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 21
- Issue
- 4
- Pages
- 223-229
- ISSN
- 1043-2760 (ISSN-L)
- 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
- 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 › Endocrinology, Diabetes and Metabolism › 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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