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Obes Rev. 2007 Nov;8(6):487-502.

Report on the IASO Stock Conference 2006: early and lifelong environmental epigenomic programming of metabolic syndrome, obesity and type II diabetes.

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  • 1Inserm U 781, Clinique Maurice Lamy, Hôpital Necker Enfants Malades 149 rue de Sèvres, Paris, France. junien@necker.fr

Abstract

Now that analysis of the organization of the human genome sequence is reaching completion, studies of the finely tuned chromatin epigenetic networks, DNA methylation and histone modifications, are required to determine how the same DNA sequence generates different cells, lineages and organs, i.e. the phenotype. Maternal nutrition, behaviour and metabolic disturbances as well as other environmental factors have been shown to have major effects on these epigenetic processes, potentially affecting the predisposition of offspring to obesity and related adult disorders. The March 2006 Stock Conference considered the latest evidence from studies in the field of obesity and other related areas that elucidate mechanisms by which the environment can modify gene expression and the resulting individual phenotype. Presentations included evaluation of the molecular basis of epigenetic memory and the nature of relevant sequence targets, windows of susceptibility, and maternal dietary and behavioural factors that determine epigenetic changes. Imprinted genes, age and tissue-related exposures, transgenerational and potential interventions were also discussed. In summary, it is clear that epigenetic alterations can no longer be ignored in evaluations of the causes of obesity and its associated disorders. There is a need for systematic large-scale epigenetic studies of obesity, employing appropriate strategies and techniques and appropriately chosen environmental factors in critical spatio-temporal windows.

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