[ brief revision on the functions of the NPY in the body]

ABSTRACT

Neuropeptide Y [NPY] is a 36 amino-acid residue peptide of pancreatic polypeptide family, which shares considerable sequence homology with PYY. It was originally isolated from porcin brain by Tatemoto et al in 1982, which is now known to be distributed throughout central and perpheral nervous systems of various species examined to date. It occurs in mammalian brain in higher concentration than all other peptides studied. It has been suggested that NPY and PYY are involved in the autonomic regulation of insulin and glucagon release. Any alteration in plasma level of the two hormones, could suggest a possible mode of action of the brain neuropeptide on the peripheral organ, specifically the islet of langerhans. NPY projections from the arcuate to medial preoptic area may be related to the central effects of this neuropeptide on luteinizing hormone release and sexual behaviour. Increasing evidence suggests a role for NPY cerebral and coronary vasospasm. The dense plexus of NPY terminal around cerebral vessels are probably responsible for NPY's potent vasoconstriction in the cerebral cortex. Coronary vesseles are also innervated heavily by NPY terminals, indicating a role for this neuropeptide in pathogenesis of coronary vasospasm. In addition, NPY affects both physiological systems and endocrine that modulate energy balance and metabolism. There are abundant evidence, particularly in rat for the involvement of NPY in the control of feeding behaviour. For example intracerebroventricular [ICV] injection of NPY, produces a strong orexigenic effect which is more enhanced by microinjection of the substance directly into the paraventricular nuclei [PVN] of the hypothalamus which receives a dense innervation of NPY containing neurons. Repeated central administration of NPY leads to continuous hyperphagia which persits, despite massive gastrointestinal distension. Existing evidence suggests that central neurochemical mechanisms involve for controlling the intake of macronutrients. In this respect it has been shown that NPY would preferentially stimulates carbohydrates and with a lesser extent fat ingestion, which develop the obesity with no significant potentiation of protein consumption. The evidences are consistant with a role for NPY in hypothalamic controle of macronutrient intake and body weight regulation, and suggest that disturbances in brain NPY may contribute to the development of eating and weight disturbances. Finally there seems to be a negative relationship between NPY and CCK petides, which is not surprising, given their opposite role in the control of feeding