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Epigenetic Changes Associated with Intrauterine Growth Retardation and Adipogenesis

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Obesity Before Birth

Part of the book series: Endocrine Updates ((ENDO,volume 30))

Abstract

Environmental contributions to the development of childhood obesity may include a suboptimal in utero environment, diabetes and/or obesity in pregnancy, and pre- and postnatal exposure to environmental chemicals, also known as obesogens. Epigenetic modifications may be one mechanism by which exposure to an altered intrauterine milieu or metabolic perturbation may influence the phenotype of the organism much later in life. Epigenetic modifications of the genome provide a mechanism that allows the stable propagation of gene expression from one generation of cells to the next. This chapter highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin remodeling and histone modifications play key roles in adipogenesis and the development of obesity. Epigenetic modifications affecting processes important to glucose regulation and insulin secretion have been described in the pancreatic β-cells and muscle of the intrauterine growth retarded (IUGR) offspring, characteristics essential to the pathophysiology of type 2 diabetes (T2DM). Epigenetic regulation of gene expression contributes to both adipocyte determination and differentiation in in vitro models. The contributions of histone acetylation, histone methylation, and DNA methylation to the process of adipogenesis in vivo remain to be evaluated.

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Pinney, S.E., Simmons, R.A. (2011). Epigenetic Changes Associated with Intrauterine Growth Retardation and Adipogenesis. In: Lustig, R. (eds) Obesity Before Birth. Endocrine Updates, vol 30. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-7034-3_8

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