Epigenetic mechanisms provide a potential explanation for how environmental influences in early life cause long-term changes in chronic disease susceptibility. Whereas epigenetic dysregulation is increasingly implicated in human developmental syndromes and cancer, the role of epigenetics in complex chronic diseases such as cardiovascular disease, type 2 diabetes and obesity remains largely uncharacterized. The inherent tissue-specificity of epigenetic regulation is the foremost impediment to an improved understanding of epigenetic dysregulation in human disease. Research in animal models is therefore crucial to enable the development of specific hypotheses that can be practicably tested in humans. We have developed a mouse model showing that methyl donor supplementation prevents transgenerational amplification of obesity, suggesting a role for DNA methylation in the developmental establishment of body weight regulation. Coupling such models with epigenomic technologies including DNA methylation-specific amplification and microarray hybridization should ultimately enable us to determine if epigenetics is an important link between early life events and adult disease.
25 - 29 Apr 2009
European Society of Endocrinology