Premium
The neuropeptide Y Y1 receptor mediates NPY‐induced inhibition of the gonadotrope axis under poor metabolic conditions
Author(s) -
Gonzales Christine,
Voirol MarieJeanne,
Giacomini Marco,
Gaillard Rolf C.,
Pedrazzini Thierry,
Pralong François P.
Publication year - 2004
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.03-0189fje
Subject(s) - neuropeptide y receptor , endocrinology , medicine , leptin , hypothalamus , receptor , biology , neuropeptide , food intake , knockout mouse , endogeny , leptin receptor , wild type , kisspeptin , chemistry , obesity , mutant , biochemistry , gene
Hypothalamic neuropeptide Y (NPY) plays a central role in the control of food intake, energy balance, and modulation of neuroendocrine functions. In particular, an increase in NPY expression participates in the inhibition of the reproductive activity under poor nutritional conditions. The present study was designed to evaluate further the involvement of the Y1 subtype of NPY receptors in these effects. Food intake, body weight gain, and the onset of puberty were studied in groups of wild‐type and Y1 deficient mice that were either fed ad libitum or subjected to a 30% restriction in food intake. This moderate feeding restriction induced a similar deficit in body weight gain in wild‐type and in Y1 knockout mice. However, although wild‐type mice experienced the expected delay of puberty, all mice in the food restriction group and lacking Y1 could go through puberty over the time of the experiment despite decreases in circulating leptin levels and increases in hypothalamic NPY expression. This observation demonstrates that the absence of Y1 impairs the perception of decreasing energy stores by the gonadotrope axis, demonstrating a physiological role for Y1 in the sensing of endogenous metabolic parameters by the hypothalamus.