The body's energy homeostasis is maintained by a highly complex and integrated neurohormonal system that minimizes fluctuations in energy balance. Neurohormones are formed by neurosecretory cells and liberated by nerve impulses (e.g., norepinephrine). Their contribution towards this energy balance includes hormonal secretion sometimes in proportion to the body fat mass and the central nervous system (CNS) targets on which these hormones act.
Of the CNS targets, a complex array of hypothalamic neuropeptides constitutes the appetite regulation system. Of these neuropeptides, NPY, a 36-amino acid orexigenic peptide, is released at the nerve terminals. In the adult rat, NPY has been observed to play a key role in affecting hyperphagia (gluttony) with resultant obesity. Various hormones orchestrate the synthesis and release of this neuropeptide. For example, pancreatic insulin and leptin released by adipocytes have been reported to suppress the synthesis and release of hypothalamic NPY, thereby potentially forming a feedback system in regulating appetite, feeding behavior, and energy balance.
A previous study demonstrated that disturbances in the fetal metabolic environment of diabetic rat or an intrauterine growth-restricted (IUGR) fetus can also alter postnatal brain NPY mRNA and peptide concentrations. This, and other research, demonstrated the presence and regulation of NPY in the fetal and neonatal hypothalamus, yet the exact functional role of this peptide during the early stages of development remains to be ascertained. Accordingly, the functional relevance of a postnatal increase in hypothalamic NPY as seen in the IUGR fetus/newborn is unknown.