Cholecystokinin and leptin act synergistically to reduce body weight
Cholecystokinin and leptin act synergistically to reduce body weight
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DOI：
10.1152/ajpregu.2000.278.4.r882
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发表时间：
2000-04-01
影响因子：
2.8
通讯作者：
Ritter, RC
中科院分区：
文献类型：
--
作者：
Matson, CA;Reid, DF;Ritter, RC
肥胖基因的产物瘦素减少大鼠和小鼠的食物摄入量和体重，而肠肽CCK的施用减少了膳食量，但没有减少体重。在目前的实验中，我们报告说，每天重复脑室内瘦素和腹腔注射CCK的组合结果显着更大的损失体重比单独瘦素。然而，瘦素加CCK治疗并没有协同减少在此期间的个人30分钟蔗糖餐的大小，和瘦素-CCK组合对每日食物摄入量的影响，而显着的，是小的强大的影响相比，对体重减轻。这种对体重减轻的协同作用依赖于CCK的外周作用和瘦素的中枢作用。这些数据表明CCK在体重调节中可能不完全依赖于进食行为的减少，并提出了一种增强瘦素抵抗性肥胖个体中瘦素作用的策略。
Leptin, the prod uct of the obese gene, reduces food intake and body weight in rats and mice, whereas administration of the gut-peptide CCK reduces meal size but not body weight. In the current experiments, we report that repeated daily combination of intracerebroventricular leptin and intraperitoneal CCK results in significantly greater loss of body weight than does leptin alone. However, leptin plus CCK treatment does not synergistically reduce the size of individual 30-min sucrose meals during this period, and the effect of leptin-CCK combination on daily chow intake, while significant, is small compared with the robust effects on body weight loss. This synergistic effect on body weight loss depends on a peripheral action of CCK and a central action of leptin. These data suggest a previously unsuspected role for CCK in body weight regulation that may not depend entirely on reduction of feeding behavior and suggest a strategy for enhancing the effects of leptin in leptin-resistant obese individuals.