Physiological Laboratory, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):8-12. doi: 10.1097/MED.0b013e32834eb77d.
Cholecystokinin (CCK) controls nutrient delivery to the small intestine by inhibiting food intake and gastric emptying. This review deals with recent work shedding new light on how and when.
Intestinal I-cells release CCK in response to dietary lipid and protein through mechanisms involving the G-protein-coupled receptors GPR40 and calcium-sensing receptor. Vagal afferent neurons are a primary target of CCK and are now recognized as an important site of integration of peripheral signals regulating ingestion. In addition to regulating vagal afferent nerve discharge, CCK also controls the expression of receptors and peptide neurotransmitters by these neurons; these actions are potentiated by leptin and inhibited by ghrelin. The responses of vagal afferent neurons to CCK are attenuated in obesity. Studies of human central nervous system responses using functional magnetic resonance imaging indicate activation of brainstem, hypothalamus and motor cortex by ingested fatty acid that is inhibited by a CCK-1 receptor antagonist. CCK may also play a role in adaptive responses in pancreatic islets by maintaining β-cell mass and acting as an incretin in certain circumstances.
CCK mediates inhibition of food intake in response to ingested lipid and protein; resistance to CCK occurs in obesity and may contribute to altered mechanisms regulating food intake.
胆囊收缩素（CCK）通过抑制摄食和胃排空来控制营养物质向小肠的输送。这篇综述探讨了最近的研究如何以及何时揭示了这一机制。
肠道 I 细胞通过涉及 G 蛋白偶联受体 GPR40 和钙敏感受体的机制，对膳食脂质和蛋白质作出反应释放 CCK。迷走传入神经是 CCK 的主要靶标，现在被认为是调节摄食的外周信号整合的重要部位。除了调节迷走传入神经放电外，CCK 还通过这些神经元控制受体和肽神经递质的表达；瘦素增强这些作用，而胃饥饿素抑制这些作用。CCK 对肥胖患者迷走传入神经元的反应减弱。使用功能磁共振成像研究人类中枢神经系统对摄入脂肪酸的反应表明，脑干、下丘脑和运动皮层被激活，而 CCK-1 受体拮抗剂则抑制了这种激活。CCK 还可能通过维持β细胞质量并在某些情况下充当肠促胰岛素在胰岛的适应性反应中发挥作用。
CCK 介导了对摄入脂质和蛋白质的摄食抑制；肥胖患者对 CCK 的反应减弱，这可能导致调节摄食的机制发生改变。
