It is possible that in IUGR, the underlying mechanisms of in utero leptin action in the developing susceptibility to adult obesity are alterations of the expression of appetite stimulating neuropeptides, such as NPY in the fetal brain [103], alterations in adipose sympathetic innervations [106], as well as an altered hypothalamic leptin receptor (ObRb, obese receptor b) expression and partitioning among the different hypothalamic nuclei [107]. Here, LEP is linked to fetal growth restriction.