ABSTRACT
The prevalence of obesity and associated disorders including type 2 diabetes is increasing globally at an alarming rate. While genetic variations in a number of genes have been linked to obesity (see Chapter 13), to date, single-nucleotide polymorphisms and copy number variations explain only a fraction of the risk of obesity and metabolic disease in humans [1]. However, there is now substantial evidence from both human and animal studies that the quality of the early-life environment before and after birth can affect susceptibility to obesity and associated metabolic disorders in later life [2]. Experimental studies show that the developmental environment can alter later phenotype by changing the epigenetic regulation of genes, and this chapter focuses on the evidence that perinatal influences such as maternal nutrition can alter epigenetic processes, leading to persistent phenotypic changes and an increased risk of childhood obesity.
