Vanderweele D A
Physiol Behav. 1982 Nov;29(5):961-4. doi: 10.1016/0031-9384(82)90352-3.
Cholecystokinin (CCK) has been shown to elicit insulin secretion and increased insulin availability has been shown to correlate with increased satiety attributed to reduced size of spontaneously occurring meals. The present experiment, however, clearly showed that CCK was effective in suppressing food ingestion in free-fed rats independent of the animal's level of insulin. Rats were tested with 1, 2 and 4 micrograms/kg of CCK-octapeptide (Sincalide, Squibb) during a baseline (pancreatic-normal) period, an insulin-poor state (streptozotocin diabetic) and an insulin clamped condition (diabetic treated by a minipump). CCK produced a highly significant (p less than 0.01) reduction of food intake compared to saline, control injections regardless of the insulin conditions of the animals. Higher doses of CCK were more effective than lower doses during all three periods of study. CCK and hyperinsulinemia function independently if they produce satiety or reductions in food intake.
胆囊收缩素（CCK）已被证明能引发胰岛素分泌，并且胰岛素可用性增加已被证明与饱腹感增加相关，这种饱腹感增加归因于自发进食量的减少。然而，本实验清楚地表明，CCK在自由进食的大鼠中能有效抑制食物摄入，且与动物的胰岛素水平无关。在基线期（胰腺正常）、胰岛素缺乏状态（链脲佐菌素糖尿病）和胰岛素钳夹状态（通过微型泵治疗的糖尿病）期间，用1、2和4微克/千克的CCK八肽（辛卡利特，施贵宝公司）对大鼠进行测试。无论动物的胰岛素状况如何，与生理盐水对照注射相比，CCK均使食物摄入量显著减少（p<0.01）。在所有三个研究阶段，较高剂量的CCK比较低剂量更有效。如果CCK和高胰岛素血症产生饱腹感或减少食物摄入量，它们的作用是独立的。
