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The epigenomic analysis of human obesity

The epigenomic analysis of human obesity
The epigenomic analysis of human obesity
The epigenome - the chemical modifications and packaging of the genome that can influence or indicate its activity - gives a molecular insight to cell-type specific workings. It can, therefore, reveal the pathophysiological mechanisms at work in disease. Detected changes can also represent physiological responses to adverse environmental exposures, thus enabling the epigenetic mark of DNA methylation to act as an epidemiological biomarker, even in surrogate tissue.
This makes epigenomic analysis an attractive prospect to further understand the pathobiology and epidemiological aspects of obesity. Furthermore, integrating epigenomic data with known obesity-associated common genetic variation can aid in deciphering their molecular mechanisms.
This review primarily examines epidemiological or population-based studies of epigenetic modifications in relation to adiposity-traits, as opposed to animal or cell models. It discusses recent work exploring the epigenome with respect to human obesity, which to date have predominately been array-based studies of DNA methylation in peripheral blood. It is of note that highly replicated BMI DNA methylation associations are not causal, but strongly driven by co-associations for more precisely measured intertwined outcomes and factors, such as hyperlipidaemia, hyperglycaemia and inflammation. Finally, the potential for the future exploration of the epigenome in obesity and related disorders will be considered.
1930-7381
1471-1481
Bell, Christopher G.
44982df7-0746-4cdb-bed1-0bdfe68f1a64
Bell, Christopher G.
44982df7-0746-4cdb-bed1-0bdfe68f1a64

Bell, Christopher G. (2017) The epigenomic analysis of human obesity. Obesity, 25 (9), 1471-1481. (doi:10.1002/oby.21909).

Record type: Article

Abstract

The epigenome - the chemical modifications and packaging of the genome that can influence or indicate its activity - gives a molecular insight to cell-type specific workings. It can, therefore, reveal the pathophysiological mechanisms at work in disease. Detected changes can also represent physiological responses to adverse environmental exposures, thus enabling the epigenetic mark of DNA methylation to act as an epidemiological biomarker, even in surrogate tissue.
This makes epigenomic analysis an attractive prospect to further understand the pathobiology and epidemiological aspects of obesity. Furthermore, integrating epigenomic data with known obesity-associated common genetic variation can aid in deciphering their molecular mechanisms.
This review primarily examines epidemiological or population-based studies of epigenetic modifications in relation to adiposity-traits, as opposed to animal or cell models. It discusses recent work exploring the epigenome with respect to human obesity, which to date have predominately been array-based studies of DNA methylation in peripheral blood. It is of note that highly replicated BMI DNA methylation associations are not causal, but strongly driven by co-associations for more precisely measured intertwined outcomes and factors, such as hyperlipidaemia, hyperglycaemia and inflammation. Finally, the potential for the future exploration of the epigenome in obesity and related disorders will be considered.

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bellcg_obesity_17_Epigenomic-Analysis-Obesity_Accepted_Manuscript - Accepted Manuscript
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More information

Accepted/In Press date: 11 May 2017
e-pub ahead of print date: 28 August 2017
Published date: September 2017
Organisations: Centre for Human Development, Stem Cells and Regeneration, Institute of Developmental Sciences, MRC Lifecourse Epidemiology Unit, Centre for Biological Sciences

Identifiers

Local EPrints ID: 411188
URI: http://eprints.soton.ac.uk/id/eprint/411188
ISSN: 1930-7381
PURE UUID: 425086f6-833a-491f-9b70-02e729994cd2
ORCID for Christopher G. Bell: ORCID iD orcid.org/0000-0003-4601-1242

Catalogue record

Date deposited: 15 Jun 2017 16:31
Last modified: 17 Dec 2019 06:06

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