PURPOSE OF REVIEW: Research suggests that 65% of variation in obesity is genetic. However, much of the known genetic associations have little known function and their effect size small, thus the gene-environment interaction, including epigenetic influences on gene expression, is suggested to be an important factor in the susceptibilty to obesity. This review will explore the potential of epigenetic markers to influence expression of genes associated with obesity. RECENT FINDINGS: Epigenetic changes in utero are known to have direct implications on the phenotype of the offspring. More recently work has focused on how such epigenetic changes continue to regulate risk of obesity from infancy through to adulthood. Work has shown that, for example, hypomethylation of the MC4 gene causes an increase in expression, and has a direct impact on appetite and intake, and thus influences risk of obesity. Similar influences are also seen in other aspects of obesity including inflammation and adiposity. SUMMARY: Maternal diet during foetal development has many epigenetic implications, which affect the offspring's risk factors for obesity during childhood and adulthood, and even in subsequent generations. Genes associated with risk of obesity, are susceptible to epigenetic mutations, which have subsequent effects on disease mechanisms, such as appetite and impaired glucose and insulin tolerance.
PURPOSE OF REVIEW: Research suggests that 65% of variation in obesity is genetic. However, much of the known genetic associations have little known function and their effect size small, thus the gene-environment interaction, including epigenetic influences on gene expression, is suggested to be an important factor in the susceptibilty to obesity. This review will explore the potential of epigenetic markers to influence expression of genes associated with obesity. RECENT FINDINGS: Epigenetic changes in utero are known to have direct implications on the phenotype of the offspring. More recently work has focused on how such epigenetic changes continue to regulate risk of obesity from infancy through to adulthood. Work has shown that, for example, hypomethylation of the MC4 gene causes an increase in expression, and has a direct impact on appetite and intake, and thus influences risk of obesity. Similar influences are also seen in other aspects of obesity including inflammation and adiposity. SUMMARY: Maternal diet during foetal development has many epigenetic implications, which affect the offspring's risk factors for obesity during childhood and adulthood, and even in subsequent generations. Genes associated with risk of obesity, are susceptible to epigenetic mutations, which have subsequent effects on disease mechanisms, such as appetite and impaired glucose and insulin tolerance.
Authors: Rodrigo San-Cristobal; Santiago Navas-Carretero; Fermín I Milagro; J Ignacio Riezu-Boj; Elizabeth Guruceaga; Carlos Celis-Morales; Katherine M Livingstone; Lorraine Brennan; Julie A Lovegrove; Hannelore Daniel; Wim H Saris; Iwonna Traczyk; Yannis Manios; Eileen R Gibney; Michael J Gibney; John C Mathers; J Alfredo Martinez Journal: J Physiol Biochem Date: 2017-03-28 Impact factor: 4.158
Authors: Terry L Davidson; Andrea L Tracy; Lindsey A Schier; Susan E Swithers Journal: J Exp Psychol Anim Learn Cogn Date: 2014-07 Impact factor: 2.478
Authors: Valentina Chiavaroli; Wayne S Cutfield; José G B Derraik; Zengxiang Pan; Sherry Ngo; Allan Sheppard; Susan Craigie; Peter Stone; Lynn Sadler; Fredrik Ahlsson Journal: Sci Rep Date: 2015-09-30 Impact factor: 4.379
Authors: Letícia A Brondani; Tais S Assmann; Bianca M de Souza; Ana P Bouças; Luis H Canani; Daisy Crispim Journal: PLoS One Date: 2014-05-07 Impact factor: 3.240