NPY Effects on Food Intake and Metabolism

The aim of this review is to critically assess the evidence that neuropeptide Y (NPY) plays both an important role in the control of food intake and in the peripheral metabolic processes linked to the obese state. When given into the brain, NPY stimulates food intake and a variety of metabolic processes that promote fat deposition. The stimulation of food intake and body weight observed with chronic administration of the peptide is persistent and leads to obesity. Both the acute and chronic stimulation of food intake and body weight produced by NPY can be reproduced with selective NPY Y1 and Y5agonists. Therefore, there is no doubt that exogenously administered NPY is a potent regulator of appetite and could be involved in the development and maintenance of obesity. However, questions remain as to whether the increase in food intake produced by exogenous NPY represents a true hunger state or is mediated by unrelated behavioral changes. Although brain NPY levels and food intake are temporally related, attempts to demonstrate a change in food intake after blockade of endogenous NPY have been mixed. Furthermore, although some studies have shown a change in food intake after blockade of NPY the conclusion that this peptide plays an important role in the control of food intake is difficult to fully accept because of the nonselective nature of the inhibitors used. Based on the available evidence our conclusion is that NPY probably plays a role in the day-to- day control of food intake. However, NPY is not a critical regulator of food intake. In its absence appetite can be controlled by a variety of other hormones and neurotransmitters. However, a definitive answer to the role played by NPY in the control of food intake and peripheral metabolism awaits the development of clean and selective inhibitors.