Christopher G Bell1,2,3,4. 1. MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK. 2. Epigenomic Medicine, Biological Sciences, Faculty of Environmental and Natural Sciences, University of Southampton, Southampton, UK. 3. Human Development and Health Academic Unit, Institute of Developmental Sciences, University of Southampton, Southampton, UK. 4. Department of Twin Research and Genetic Epidemiology, King's College London, London, UK.
Abstract
OBJECTIVE: Analysis of the epigenome-the chemical modifications and packaging of the genome that can influence or indicate its activity-enables molecular insight into cell type-specific machinery. 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. METHODS AND CONCLUSIONS: 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 has predominately consisted of 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 coassociations for more precisely measured intertwined outcomes and factors, such as hyperlipidemia, hyperglycemia, and inflammation. Finally, the potential for the future exploration of the epigenome in obesity and related disorders is considered.
OBJECTIVE: Analysis of the epigenome-the chemical modifications and packaging of the genome that can influence or indicate its activity-enables molecular insight into cell type-specific machinery. 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. METHODS AND CONCLUSIONS: 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 humanobesity, which to date has predominately consisted of 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 coassociations for more precisely measured intertwined outcomes and factors, such as hyperlipidemia, hyperglycemia, and inflammation. Finally, the potential for the future exploration of the epigenome in obesity and related disorders is considered.
Authors: E Makrinou; A W Drong; G Christopoulos; A Lerner; I Chapa-Chorda; T Karaderi; S Lavery; K Hardy; C M Lindgren; S Franks Journal: Mol Cell Endocrinol Date: 2019-10-07 Impact factor: 4.102
Authors: Rafaella Cristhine Pordeus Luna; Mayara Karla Dos Santos Nunes; Mussara Gomes Cavalcante Alves Monteiro; Cássia Surama Oliveira da Silva; Rayner Anderson Ferreira do Nascimento; Raquel Patrícia Ataíde Lima; Flávia Cristina Fernandes Pimenta; Naila Francis Paulo de Oliveira; Darlene Camati Persuhn; Aléssio Tony Cavalcanti de Almeida; Alcides da Silva Diniz; Cristina Wide Pissetti; Rodrigo Pinheiro Toledo Vianna; Flavia Emília Leite de Lima Ferreira; Maria da Conceição Rodrigues Gonçalves; Maria José de Carvalho Costa Journal: Nutr Metab (Lond) Date: 2018-07-11 Impact factor: 4.169