Mouse models have suggested that IUGR may lead to a decreased anorexic response to leptin, central dysregulation of appetite and abnormal adipocyte activation, increasing their risk of developing obesity later in life.99,100 Similarly, animal studies have shown that altered intracellular insulin signalling pathways and reduced number of pancreatic islet cells in IUGR increase the likelihood of developing glucose intolerance.101,102 All these maladaptive foetal programming secondary to IUGR leads to an increased risk of developing CVD, obesity and T2D. This evidence concerns the gene LEP and fetal growth restriction.