Considering that (1) IUGR is one of the main risk factors for developing non-obese T2DM, (2) fetal programing of the central nervous system contributes primarily to the development of the IUGR phenotype, (3) the role of hypothalamic NUCB2/nesfatin-1 in the regulation of food intake and glucose homeostasis is established and that (4) nesfatin-1 acts in a leptin independent manner, the role of NUCB2/nesfatin-1 in the development of the non-obese type T2DM in the IUGR phenotype can be assumed. The gene discussed is LEP; the disease is fetal growth restriction.