Donovan Michael J, Paulino Gabriel, Raybould Helen E
Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California Davis, California 95616, United States.
Physiol Behav. 2007 Dec 5;92(5):969-74. doi: 10.1016/j.physbeh.2007.07.003.
Cholecystokinin (CCK), released by lipid in the intestine, initiates satiety by acting at cholecystokinin type 1 receptors (CCK(1)Rs) located on vagal afferent nerve terminals located in the wall of the gastrointestinal tract. In the present study, we determined the role of the CCK(1)R in the short term effects of a high fat diet on daily food intake and meal patterns using mice in which the CCK(1)R gene is deleted. CCK(1)R(-/-) and CCK(1)R(+/+) mice were fed isocaloric high fat (HF) or low fat (LF) diets ad libitum for 18 h each day and meal size, meal frequency, intermeal interval, and meal duration were determined. Daily food intake was unaltered by diet in the CCK(1)R(-/-) compared to CCK(1)R(+/+) mice. However, meal size was larger in the CCK(1)R(-/-) mice compared to CCK(1)R(+/+) mice when fed a HF diet, with a concomitant decrease in meal frequency. Meal duration was increased in mice fed HF diet regardless of phenotype. In addition, CCK(1)R(-/-) mice fed a HF diet had a 75% decrease in the time to 1st meal compared to CCK(1)R(+/+) mice following a 6 h fast. These data suggest that lack of the CCK(1)R results in diminished satiation, causing altered meal patterns including larger, less frequent meals when fed a high fat diet. These results suggest that the CCK(1)R is involved in regulating caloric intake on a meal to meal basis, but that other factors are responsible for regulation of daily food intake.
胆囊收缩素（CCK）由肠道中的脂质释放，通过作用于位于胃肠道壁迷走神经传入神经末梢上的1型胆囊收缩素受体（CCK(1)Rs）引发饱腹感。在本研究中，我们使用CCK(1)R基因缺失的小鼠，确定了CCK(1)R在高脂饮食对每日食物摄入量和进食模式的短期影响中的作用。CCK(1)R(-/-)和CCK(1)R(+/+)小鼠每天随意进食等热量的高脂（HF）或低脂（LF）饮食18小时，并测定每餐食量、进餐频率、餐间间隔和进餐持续时间。与CCK(1)R(+/+)小鼠相比，CCK(1)R(-/-)小鼠的每日食物摄入量不受饮食影响。然而，喂食HF饮食时，CCK(1)R(-/-)小鼠的每餐食量比CCK(1)R(+/+)小鼠大，同时进餐频率降低。无论表型如何，喂食HF饮食的小鼠进餐持续时间均增加。此外，禁食6小时后，喂食HF饮食的CCK(1)R(-/-)小鼠与CCK(1)R(+/+)小鼠相比，首次进餐时间减少了75%。这些数据表明，CCK(1)R的缺失导致饱腹感降低，从而改变进食模式，包括喂食高脂饮食时食量更大、进餐频率更低。这些结果表明，CCK(1)R参与逐餐调节热量摄入，但其他因素负责调节每日食物摄入量。
