Energy metabolism and turnover are increased in mice lacking the cholecystokinin-B receptor

被引:38
作者
Miyasaka, K [1 ]
Ichikawa, M
Ohta, M
Kanai, S
Yoshida, Y
Masuda, M
Nagata, A
Matsui, S
Noda, T
Takiguchi, S
Takata, Y
Kawanami, T
Funakoshi, A
机构
[1] Tokyo Metropolitan Inst Gerontol, Dept Clin Physiol, Tokyo 1730015, Japan
[2] Kobe Univ, Sch Med, Dept Internal Med 3, Kobe, Hyogo 650, Japan
[3] Tohoku Univ, Sch Med, Dept Mol Genet, Sendai, Miyagi 9808575, Japan
[4] Kyushu Natl Canc Ctr, Res Inst, Fukuoka 8111395, Japan
[5] Kyushu Natl Canc Ctr, Dept Gastroenterol, Fukuoka 8111395, Japan
关键词
energy expenditure; energy intake; energy metabolism; knockout mice; cholecystokinin-receptor;
D O I
10.1093/jn/132.4.739
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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.
引用
收藏
页码:739 / 741
页数:3
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