In maternal low-protein animal models of later life obesity, alterations of the methylation status in the promoter of metabolic genes, such as hepatic PPARα, glucocorticoid receptor (GR), and liver X receptor (LXR) and hypomethylation of leptin promoter in adipose tissue have been reported during fetal and postnatal life [115], highlighting the importance of in utero environment as a predeterminant of later life chromatin function. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.