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First published on November 14, 2006; DOI: 10.1124/mol.106.029991

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Received for publication August 16, 2006.
Revised November 8, 2006.
Accepted for publication November 14, 2006.

A pair-feeding study reveals that a Y5 antagonist causes weight loss in diet-induced obese mice by modulating food intake and energy expenditure

Satoshi Mashiko 1, Akane Ishihara 1, Hisashi Iwaasa 1, Hideki Sano 1, Junko Ito 1, Akira Gomori 1, Zenjun Oda 1, Ryuichi Moriya 1, Hiroko Matsushita 1, Makoto Jitsuoka 1, Osamu Okamoto 1, Douglas J MacNeil 2, Lex HT van der Ploeg 2, Takehiro Fukami 1, Akio Kanatani 1*

1 Banyu Tsukuba Research Institute 2 Merck Research Laboratories

* Address correspondence to: E-mail: akio_kanatani{at}merck.com

Abstract

NPY is thought to have a significant role in the physiological control of energy homeostasis. We recently reported that an NPY Y5 antagonist inhibits body weight gain in diet-induced obese (DIO) mice, with a moderate reduction in food intake. In order to clarify the mechanism of the anti-obesity effects of the Y5 antagonist, we conducted a pair-feeding study in DIO mice. The Y5 antagonist at 100 mg/kg produced a moderate feeding suppression leading to an 18% decrease in body weight, without altering body temperature. In contrast, the pair-fed group showed only a transient weight reduction and a reduced body temperature, thus indicating that the Y5 antagonist stimulates thermogenesis. The Y5 antagonist-treated mice showed an up-regulation of uncoupling protein mRNA in brown adipose tissue (BAT) and white adipose tissue (WAT), suggesting that both BAT and WAT contribute to energy expenditure. Thus, the Y5 antagonist induces its anti-obesity effects by acting on both energy intake and expenditure.


Key words: NPY, Neuropeptides, peptidases


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