These alterations are accompanied by metabolic and gene expression changes, including overexpression of the hepatic glucocorticoid and PParα receptors, and epigenetic changes that facilitate transcription of these receptors: For the glucocorticoid receptor, these changes include histone modifications as shown in a model of IUGR obtained by bilateral uterine ligation [50]. This evidence concerns the gene NR3C1 and fetal growth restriction.