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Am J Physiol Endocrinol Metab (January 28, 2003). doi:10.1152/ajpendo.00529.2002
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Submitted on December 4, 2002
Accepted on January 23, 2003

Characterization of MCH-mediated obesity in mice

Masahiko Ito1, Akira Gomori1, Akane Ishihara1, Zenjun Oda1, Satoshi Mashiko1, Hiroko Matsushita1, Mariko Yumoto1, Makoto Ito1, Hideki Sano1, Shigeru Tokita1, Minoru Moriya1, Hisashi Iwaasa1*, and Akio Kanatani1

1 Tsukuba Research Institute, Banyu Pharmaceutical Co., Ltd., Tsukuba, Ibaraki, Japan

* To whom correspondence should be addressed. E-mail: iwaasahs{at}banyu.co.jp.

Melanin-concentrating hormone (MCH) is a cyclic orexigenic peptide expressed in the lateral hypothalamus. Recently, we demonstrated that chronic intracerebroventricular infusion of MCH induced obesity accompanied by sustained hyperphagia in mice. Here we analyzed the mechanism of MCH-induced obesity by comparing animals fed ad libitum (ad lib) with pair-fed and control animals. Chronic infusion of MCH significantly increased food intake, body weight, white adipose tissue (WAT) mass, and liver mass in ad lib fed mice on a moderately high fat diet. In addition, a significant increase in lipogenic activity was observed in the WAT of the ad lib fed group. Although body weight gain was marginal in the pair-fed group, MCH infusion clearly enhanced the lipogenic activity in liver and WAT. Plasma leptin levels were also increased in the pair-fed group. Furthermore, MCH infusion significantly reduced rectal temperatures in the pair-fed group. In support of these findings, mRNA expression of uncoupling protein-1, acyl-CoA oxidase, and carnitine-palmitoyl transferase-1, which are key molecules involved in thermogenesis and fatty acid oxidation, were reduced in the brown adipose tissue (BAT) of the pair-fed group suggesting that MCH-infusion might reduce BAT functions. We conclude that the activation of MCH neuronal pathways stimulated adiposity, in part resulting from increased lipogenesis in liver and WAT and reduced energy expenditure in BAT. These findings confirm that modulation of energy homeostasis by MCH may play a critical role in the development of obesity.




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