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Nutrient Metabolism
Research Communication

Energy Metabolism and Turnover Are Increased in Mice Lacking the Cholecystokinin-B Receptor¹

Kyoko Miyasaka^*2, Mineko Ichikawa, Minoru Ohta^*, Setsuko Kanai^*, Yuki Yoshida^*, Masao Masuda^*, Aki Nagata^**, Toshimitsu Matsui^**, Tetsuo Noda, Soichi Takiguchi, Yutaka Takata, Takako Kawanami and Akihiro Funakoshi

^* Department of Clinical Physiology and Nutrition, Tokyo Metropolitan Institute of Gerontology, Tokyo-l73–0015, Japan; ^** Third Department of Internal Medicine, Kobe University School of Medicine, Kobe-650, Japan; Department of Molecular Genetics, Tohoku University School of Medicine, Sendai-980–8575, Japan; and Research Institute and Department of Gastroenterology, National Kyushu Cancer Center, Fukuoka-811–1395, Japan

²To whom correspondence should be addressed. E-mail: miyasaka{at}tmig.or.jp.

Cholecystokinin (CCK) is an important gastrointestinal hormone as well as a neurotransmitter. Two types of CCK receptors, types A and B, have been identified. The CCK-A receptor is involved in satiety, food intake and behavior, whereas the B receptor is involved in anxiety. We recently produced CCK-A, -B and AB receptor knockout mice to study the role of these receptors in energy metabolism. Daily energy intake and expenditure were significantly greater in CCK-BR(-/-) and CCK-AR(-/-)BR(-/-) mice than CCK-AR(-/-) and wild-type [CCK-AR(+/+)BR(+/+)] mice. Relative liver and kidney weights (g/kg body) were significantly greater in CCK-AR(-/-)BR(-/-) mice than in wild-type mice. Energy metabolism and energy turnover were increased in mice with a disruption of the CCK-BR gene, although the underlying mechanism is unknown.

KEY WORDS: • energy expenditure • energy intake • energy metabolism • knockout mice • cholecystokinin-receptor

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