地伐西匹改变了瘦型雄性 Zucker 大鼠的进食模式，但对肥胖型雄性 Zucker 大鼠无效。

Devazepide alters meal patterns in lean, but not obese, male Zucker rats.

作者信息

Strohmayer A J, Greenberg D

机构信息

Department of Neurology, North Shore University Hospital-Cornell University Medical College, New York, NY.

出版信息

Physiol Behav. 1994 Nov;56(5):1037-9. doi: 10.1016/0031-9384(94)90340-9.

DOI:10.1016/0031-9384(94)90340-9

PMID:7824568

Abstract

Meal patterns were recorded for 10.5 h in six lean and eight obese adult male Zucker rats after treatment with the cholecystokinin type A (CCKA) receptor antagonist, devazepide (750 micrograms/kg, IP, at 1330 h) or vehicle. In lean rats, devazepide significantly increased total food intake by 11%, average meal size by 35%, and meal duration by 49%. Devazepide also significantly decreased the average number of meals by 18%, although this was a smaller effect. Devazepide had none of these effects in obese rats. Devazepide treatment altered the meal pattern of lean rats so that it was similar to that of obese rats. These results demonstrate that endogenous CCK has a satiating effect in lean, but not in obese, male Zucker rats, which is the first demonstration of a loss of a physiological satiety signal in the obese Zucker rat. This defect could be due to: 1) a decrease in the release of endogenous CCK, 2) a decrease in the rate of CCK synthesis, or 3) the production of an abnormal form of CCK.

摘要

给六只瘦型成年雄性 Zucker 大鼠和八只肥胖成年雄性 Zucker 大鼠注射 A 型胆囊收缩素（CCKA）受体拮抗剂地伐西匹（750 微克/千克，腹腔注射，于 1330 时）或赋形剂后，记录它们 10.5 小时的进食模式。在瘦型大鼠中，地伐西匹使总食物摄入量显著增加了 11%，平均餐量增加了 35%，进餐持续时间增加了 49%。地伐西匹还使平均进餐次数显著减少了 18%，尽管这一影响较小。地伐西匹对肥胖大鼠没有这些作用。地伐西匹治疗改变了瘦型大鼠的进食模式，使其与肥胖大鼠的进食模式相似。这些结果表明，内源性 CCK 在瘦型雄性 Zucker 大鼠中有饱腹感作用，但在肥胖雄性 Zucker 大鼠中没有，这是首次证明肥胖 Zucker 大鼠生理饱腹感信号缺失。这种缺陷可能是由于：1）内源性 CCK 释放减少；2）CCK 合成速率降低；或 3）产生了异常形式的 CCK。