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Am J Physiol 1999 Nov;277(5 Pt 2):R1428-R1434
Activation of the NPY Y5 receptor regulates both feeding and energy
expenditure.
Hwa JJ, Witten MB, Williams P, Ghibaudi L, Gao J, Salisbury BG, Mullins D, Hamud F, Strader CD, Parker EM
Department of CNS and Cardiovascular Research, Schering-Plough Research Institute, Kenilworth, New Jersey 07033.
[Record supplied by publisher]
Intracerebroventricular (ICV) administration of neuropeptide Y (NPY) has been shown to decrease energy expenditure, induce
hypothermia, and stimulate food intake. Recent evidence has suggested that the Y5 receptor may be a significant mediator of
NPY-stimulated feeding. The present study attempts to further characterize the role of NPY Y5-receptor subtypes in feeding
and energy expenditure regulation. Satiated Long-Evans rats with temperature transponders implanted in the interscapular
brown adipose tissue (BAT) displayed a dose-dependent decrease in BAT temperature and an increase in food intake after
ICV infusion of NPY. Similar effects were induced by ICV administration of peptide analogs of NPY that activate the Y5
receptor, but not by analogs that activate Y1, Y2, or Y4 receptors. Furthermore, ICV infusion of the Y5 selective agonist
D--NPY significantly reduced oxygen consumption and energy expenditure of rats as measured by indirect
calorimetry. These data suggest that the NPY Y5-receptor subtype not only mediates the feeding response of NPY but also
contributes to brown fat temperature and energy expenditure regulation. |
