Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia
Open accessAbstract
The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains <25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB–induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced α-oxoaldehydes. These results highlight the dramatic and long-lasting effects that short-term hyperglycemic spikes can have on vascular cells and suggest that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications.
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Histone modifications regulate the expression of genes implicated in diabetic complications.
“Whilst DNA methylation modifications are believed to confer ‘metabolic memory’ other studies indicate histone modifications regulate the expression of genes implicated in diabetic complications 98, 99.”
From The Circadian Syndrome: is the Metabolic Syndrome and much more! (2019) · cites this paper as [98]
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- Authors
- El-Osta, A., Brasacchio, D., Yao, D., Pocai, A., Jones, P. L., Roeder, R. G., Cooper, M. E., & Brownlee, M.
- Affiliations
- 1Diabetes and Metabolism Division, Baker Epigenetics in Human Health and Disease, and
- Breakthrough T1D (US)
- Albert Einstein College of Medicine (US)
- University of Illinois Urbana-Champaign (US)
- Rockefeller University (US)
- Baker Heart and Diabetes Institute (AU)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2008-09-22
- Volume
- 205
- Issue
- 10
- Pages
- 2409-2417
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2556800
- OpenAlex
- W2123212032
- Cited by
- 1,115
- References
- 33
- Citations by year
- 2026: 55 · 2025: 45 · 2024: 57 · 2023: 46 · 2022: 52 · 2021: 74 · 2020: 71 · 2019: 45 · 2018: 72 · 2017: 60 · 2016: 67 · 2015: 91 · 2014: 76 · 2013: 73 · 2012: 72
- FWCI
- 35.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-sa)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion, cc-by-nc-sa)
- Funders
- COMSATS Institute of Information Technology
- National Heart Foundation of Australia
- Directorate for Biological Sciences
- Medical Research Council
- National Health and Medical Research Council
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 060764, R01DK060764)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- transient hyperglycemia, glycemic variability, NF-κB p65, epigenetic modifications, promoter activation, aortic endothelial cells, MCP-1, VCAM-1, mitochondrial superoxide, alpha-oxoaldehydes, diabetes complications
- MeSH terms
- Uncoupling Protein 1, Histone Methyltransferases, Animals, Blood Glucose, Cattle, Cells, Cultured, Diabetes Mellitus, Gene Expression Regulation, Glucose, Glycated Hemoglobin, Humans, Hyperglycemia, Ion Channels, Male, Mice, Inbred C57BL, Mitochondria, Promoter Regions, Genetic, Histone-Lysine N-Methyltransferase, Protein Methyltransferases, Risk Factors, Superoxide Dismutase, Reactive Oxygen Species, Mice, Knockout, Chemokine CCL2, Vascular Cell Adhesion Molecule-1, Mitochondrial Proteins, Endothelial Cells, Epigenesis, Genetic, Diabetes Complications, Mice, Transcription Factor RelA
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