Pappas T N
Department of Surgery, Duke University Medical Center, Durham, NC.
Am J Clin Nutr. 1992 Feb;55(2 Suppl):571S-572S. doi: 10.1093/ajcn/55.2.571s.
This manuscript reviews the known satiety signals and the impact of antiobesity surgery on these physiological satiety mechanisms. Satiety signals originate from the stomach and small bowel to stop eating behavior. Stomach signals (gastric distension) produce early satiety by releasing hypothalamic cholecystokinin (CCK). The intermeal interval is probably mediated by peripheral CCK released by a threshold level of intraluminal calories. Anti-obesity operations probably rely little on these physiological satiety signals. Gastric balloons and gastroplasty produce nonphysiological gastric distension whereas intestinal bypass causes malabsorption. Gastric bypass combines supramaximal gastric distension with taste aversion from dumping. Future physiological manipulation of the satiety cascade will lead to improve obesity intervention.
本手稿回顾了已知的饱腹感信号以及减肥手术对这些生理饱腹感机制的影响。饱腹感信号源自胃和小肠，以停止进食行为。胃信号（胃扩张）通过释放下丘脑胆囊收缩素（CCK）产生早期饱腹感。餐间间隔可能由腔内热量的阈值水平释放的外周CCK介导。减肥手术可能很少依赖这些生理饱腹感信号。胃内气球和胃成形术会产生非生理性胃扩张，而肠道分流会导致吸收不良。胃旁路手术将超最大胃扩张与倾倒引起的味觉厌恶相结合。未来对饱腹感级联的生理操纵将改善肥胖干预。
