The role of global and regional DNA methylation and histone modifications in glycemic traits and type 2 diabetes: A systematic review

T. Muka, J. Nano, T. Voortman, K. V.E. Braun, S. Ligthart, S. Stranges, W. M. Bramer, J. Troup, R. Chowdhury, A. Dehghan, O. H. Franco

Research output: Contribution to journalReview articleAcademicpeer-review

24 Citations (Scopus)

Abstract

Background: New evidence suggests the potential involvement of epigenetic mechanisms in type 2 diabetes (T2D) as a crucial interface between the effects of genetic predisposition and environmental influences. Aim: To systematically review studies investigating the association between epigenetic marks (DNA methylation and histone modifications) with T2D and glycemic traits (glucose and insulin levels, insulin resistance measured by HOMA-IR). Method and Results: Six bibliographic databases (Embase.com, Medline (Ovid), Web-of-Science, PubMed, Cochrane Central and Google Scholar) were screened until 28th August 2015. We included randomized controlled trials, cohort, case-control and cross-sectional studies in humans that examined the association between epigenetic marks (global, candidate or genome-wide methylation of DNA and histone modifications) with T2D, glucose and insulin levels and insulin metabolism.Of the initially identified 3879 references, 53 articles, based on 47 unique studies met our inclusion criteria. Overall, data were available on 10,823 participants, with a total of 3358 T2D cases. There was no consistent evidence for an association between global DNA-methylation with T2D, glucose, insulin and insulin resistance. The studies reported epigenetic regulation of several candidate genes for diabetes susceptibility in blood cells, muscle, adipose tissue and placenta to be related with T2D without any general overlap between them. Histone modifications in relation to T2D were reported only in 3 observational studies. Conclusions and relevance: Current evidence supports an association between epigenetic marks and T2D. However, overall evidence is limited, highlighting the need for further larger-scale and prospective investigations to establish whether epigenetic marks may influence the risk of developing T2D.

Original languageEnglish
Pages (from-to)553-566
Number of pages14
JournalNutrition, Metabolism and Cardiovascular Diseases
Volume26
Issue number7
DOIs
Publication statusPublished - 1 Jul 2016
Externally publishedYes

Fingerprint

Histone Code
DNA Methylation
Type 2 Diabetes Mellitus
Epigenomics
Insulin
Glucose
Insulin Resistance
Bibliographic Databases
Genetic Predisposition to Disease
PubMed
Placenta
Observational Studies
Adipose Tissue
Blood Cells
Randomized Controlled Trials
Cross-Sectional Studies
Genome

Keywords

  • Epigenetics
  • Global DNA methylation
  • Glucose
  • Histone modification
  • Insulin
  • Insulin resistance
  • Type 2 diabetes

Cite this

Muka, T. ; Nano, J. ; Voortman, T. ; Braun, K. V.E. ; Ligthart, S. ; Stranges, S. ; Bramer, W. M. ; Troup, J. ; Chowdhury, R. ; Dehghan, A. ; Franco, O. H. / The role of global and regional DNA methylation and histone modifications in glycemic traits and type 2 diabetes : A systematic review. In: Nutrition, Metabolism and Cardiovascular Diseases. 2016 ; Vol. 26, No. 7. pp. 553-566.
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Muka, T, Nano, J, Voortman, T, Braun, KVE, Ligthart, S, Stranges, S, Bramer, WM, Troup, J, Chowdhury, R, Dehghan, A & Franco, OH 2016, 'The role of global and regional DNA methylation and histone modifications in glycemic traits and type 2 diabetes: A systematic review' Nutrition, Metabolism and Cardiovascular Diseases, vol. 26, no. 7, pp. 553-566. https://doi.org/10.1016/j.numecd.2016.04.002

The role of global and regional DNA methylation and histone modifications in glycemic traits and type 2 diabetes : A systematic review. / Muka, T.; Nano, J.; Voortman, T.; Braun, K. V.E.; Ligthart, S.; Stranges, S.; Bramer, W. M.; Troup, J.; Chowdhury, R.; Dehghan, A.; Franco, O. H.

In: Nutrition, Metabolism and Cardiovascular Diseases, Vol. 26, No. 7, 01.07.2016, p. 553-566.

Research output: Contribution to journalReview articleAcademicpeer-review

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T1 - The role of global and regional DNA methylation and histone modifications in glycemic traits and type 2 diabetes

T2 - A systematic review

AU - Muka, T.

AU - Nano, J.

AU - Voortman, T.

AU - Braun, K. V.E.

AU - Ligthart, S.

AU - Stranges, S.

AU - Bramer, W. M.

AU - Troup, J.

AU - Chowdhury, R.

AU - Dehghan, A.

AU - Franco, O. H.

PY - 2016/7/1

Y1 - 2016/7/1

N2 - Background: New evidence suggests the potential involvement of epigenetic mechanisms in type 2 diabetes (T2D) as a crucial interface between the effects of genetic predisposition and environmental influences. Aim: To systematically review studies investigating the association between epigenetic marks (DNA methylation and histone modifications) with T2D and glycemic traits (glucose and insulin levels, insulin resistance measured by HOMA-IR). Method and Results: Six bibliographic databases (Embase.com, Medline (Ovid), Web-of-Science, PubMed, Cochrane Central and Google Scholar) were screened until 28th August 2015. We included randomized controlled trials, cohort, case-control and cross-sectional studies in humans that examined the association between epigenetic marks (global, candidate or genome-wide methylation of DNA and histone modifications) with T2D, glucose and insulin levels and insulin metabolism.Of the initially identified 3879 references, 53 articles, based on 47 unique studies met our inclusion criteria. Overall, data were available on 10,823 participants, with a total of 3358 T2D cases. There was no consistent evidence for an association between global DNA-methylation with T2D, glucose, insulin and insulin resistance. The studies reported epigenetic regulation of several candidate genes for diabetes susceptibility in blood cells, muscle, adipose tissue and placenta to be related with T2D without any general overlap between them. Histone modifications in relation to T2D were reported only in 3 observational studies. Conclusions and relevance: Current evidence supports an association between epigenetic marks and T2D. However, overall evidence is limited, highlighting the need for further larger-scale and prospective investigations to establish whether epigenetic marks may influence the risk of developing T2D.

AB - Background: New evidence suggests the potential involvement of epigenetic mechanisms in type 2 diabetes (T2D) as a crucial interface between the effects of genetic predisposition and environmental influences. Aim: To systematically review studies investigating the association between epigenetic marks (DNA methylation and histone modifications) with T2D and glycemic traits (glucose and insulin levels, insulin resistance measured by HOMA-IR). Method and Results: Six bibliographic databases (Embase.com, Medline (Ovid), Web-of-Science, PubMed, Cochrane Central and Google Scholar) were screened until 28th August 2015. We included randomized controlled trials, cohort, case-control and cross-sectional studies in humans that examined the association between epigenetic marks (global, candidate or genome-wide methylation of DNA and histone modifications) with T2D, glucose and insulin levels and insulin metabolism.Of the initially identified 3879 references, 53 articles, based on 47 unique studies met our inclusion criteria. Overall, data were available on 10,823 participants, with a total of 3358 T2D cases. There was no consistent evidence for an association between global DNA-methylation with T2D, glucose, insulin and insulin resistance. The studies reported epigenetic regulation of several candidate genes for diabetes susceptibility in blood cells, muscle, adipose tissue and placenta to be related with T2D without any general overlap between them. Histone modifications in relation to T2D were reported only in 3 observational studies. Conclusions and relevance: Current evidence supports an association between epigenetic marks and T2D. However, overall evidence is limited, highlighting the need for further larger-scale and prospective investigations to establish whether epigenetic marks may influence the risk of developing T2D.

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KW - Global DNA methylation

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KW - Histone modification

KW - Insulin

KW - Insulin resistance

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