De Fanti B A, Backus R C, Hamilton J S, Gietzen D W, Horwitz B A
Division of Biological Sciences: Neurobiology, Physiology, and Behavior, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
Am J Physiol. 1998 Jul;275(1):E1-5. doi: 10.1152/ajpendo.1998.275.1.E1.
Neuropeptides play an important role in the integration of dietary signals. Cholecystokinin (CCK) has been implicated in regulating ingestive behavior, particularly satiety. The primary objective of this study was to examine whether the hyperphagia characteristic of obese (fa/fa) rats involves impaired neural CCK secretion. Dynamic release of CCK at the hypothalamic paraventricular nucleus (PVN) of age-matched lean (Fa/Fa) and obese Zucker rats was determined using push-pull perfusion. The gavage of a 10.3-kcal (6 ml) liquid diet during lights off was followed by increased CCK release in lean rats (from 13.6 +/- 1.1 to 22.1 +/- 1.4 fmol in the 1st postprandial period and 18.4 +/- 2.5 fmol in the 2nd postprandial period). An identical meal load resulted in no postprandial increase in CCK release in obese rats, despite the fact that high-K+ artificial cerebrospinal fluid evoked CCK outflow in all animals. Intubation of 6 ml of nonnutritive 1% carboxymethylcellulose had no effect. These results are consistent with the suggestion that hypothalamic CCK plays a physiological role in satiety, and they demonstrate that obese Zucker rats have blunted hypothalamic CCK release in response to dietary cues.
神经肽在饮食信号整合中发挥重要作用。胆囊收缩素（CCK）与调节摄食行为，尤其是饱腹感有关。本研究的主要目的是检验肥胖（fa/fa）大鼠的多食特征是否涉及神经CCK分泌受损。使用推挽灌注法测定年龄匹配的瘦型（Fa/Fa）和肥胖型 Zucker 大鼠下丘脑室旁核（PVN）中 CCK 的动态释放。在熄灯期间给瘦型大鼠灌胃 10.3 千卡（6 毫升）液体饮食后，CCK 释放增加（餐后第 1 期从 13.6±1.1 飞摩尔增加到 22.1±1.4 飞摩尔，餐后第 2 期为 18.4±2.5 飞摩尔）。相同的进餐量在肥胖大鼠中并未导致餐后 CCK 释放增加，尽管高钾人工脑脊液能引起所有动物的 CCK 流出。插管注入 6 毫升非营养性 1%羧甲基纤维素没有效果。这些结果与下丘脑 CCK 在饱腹感中发挥生理作用的观点一致，并且表明肥胖 Zucker 大鼠对饮食线索的下丘脑 CCK 释放反应迟钝。
