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- Miyasaka Kyoko
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Kanai Setsuko
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Ohta Minoru
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Hosoya Hiroko
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Takano Saeko
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Sekime Ayako
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Sakurai Chihiro
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Kaneko Takao
- Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology
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- Tahara Shoichi
- Redox Regulation Research Group, Tokyo Metropolitan Institute of Gerontology
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- Funakoshi Akihiro
- Division of Gastroenterology, Kyushu Cancer Center
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抄録
In mammals, including humans, a brain-gut hormone, cholecystokinin (CCK) mediates the satiety effect via CCK-A receptor (R). We generated CCK-AR gene-deficient (−/−) mice and found that the daily food intake, energy expenditure, and gastric emptying of a liquid meal did not change compared with those of wild-type mice. Because CCK-AR(−/−) mice show anxiolytic status, we examined the effects of restraint stress. Seven hours of restraint stress was found to significantly decrease both body weight and food intake during the subsequent 3 days in all tested animals. On the fourth day after restraint stress, the CCK-AR(−/−) mice showed a significantly higher level of daily food intake than prior to stress, and food intake recovered to prestress levels in the wild-type mice. Since peripheral CCK-AR has been known to mediate gastric emptying, both gastric emptying and gastric acid secretion were determined to examine the mechanism of overeating in CCK-AR(−/−) mice. Neither gastric emptying nor gastric acid secretion differed between CCK-AR(−/−) and wild-type mice on the fourth day after stress. In contrast, however, the contents of dopamine and its metabolites in the cerebral cortex of CCK-AR(-/-) mice were increased by stress, but were rather decreased in wild-type mice. Changes in 5-hydroxytryptamine (5-HT) and its metabolite 5HIAA did not differ between the genotypes. In conclusion, CCK-AR(−/−) mice showed overeating after restraint stress, and dopaminergic hyperfunction in the brain of these mice was observed. The present evidence suggests that the CCK-AR function, possibly via altering the dopaminergic function, might be involved in overeating after stress.<br>
収録刊行物
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- The Japanese Journal of Physiology
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The Japanese Journal of Physiology 55 (5), 285-291, 2005
一般社団法人 日本生理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205041173120
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- NII論文ID
- 10018623962
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- NII書誌ID
- AA00691224
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- ISSN
- 18811396
- 0021521X
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- NDL書誌ID
- 7836866
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
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- 抄録ライセンスフラグ
- 使用不可