Gibbs J, Smith G P
Department of Psychiatry, Cornell University Medical College, White Plains, N.Y.
Ann Endocrinol (Paris). 1988;49(2):113-20.
The systemic administration of exogenous cholecystokinin (CCK), (a peptide released into the circulation when nutrients arrive in small intestine) provokes inhibition of food intake in numerous animal species and a sensation of satiation in humans. The mechanism involved requires participation of vagal afferent neurons to transmit information, possibly on gastric distension, to brain stem. Two crucial questions remain unanswered: does peripheral endogenous cholecystokinin transport information necessary for satiation at end of normal meals and if so, how and when is this message coded and deciphered; other studies have demonstrated that very small doses of exogenous cholecystokinin (too low to induce satiation if administrated peripherally) will induce satiety if injected into cerebral ventricles or directly into cerebral parenchyma. This suggest but does not prove that cerebral endogenous CCK also plays a role in satiety. It is not known how the satiating action of centrally-administered CCK is related to that of peripherally-administered CCK. Current studies aim at establishing a coherent schema of neuro-endocrine mechanisms implicated (from the gastrointestinal wall via the brain to a motivated behaviour) in the fact that food taken during a meal induces the end of the latter.
外源性胆囊收缩素（CCK）（一种当营养物质进入小肠时释放到循环系统中的肽）的全身给药会抑制多种动物的食物摄入，并在人类中引起饱腹感。其中涉及的机制需要迷走神经传入神经元参与，将可能关于胃扩张的信息传递到脑干。两个关键问题仍未得到解答：外周内源性胆囊收缩素是否传递正常进餐结束时饱腹感所需的信息，如果是，该信息如何以及何时被编码和解码；其他研究表明，非常小剂量的外源性胆囊收缩素（如果外周给药则剂量过低无法诱导饱腹感）如果注入脑室或直接注入脑实质会诱导饱腹感。这表明但并未证明脑内源性CCK在饱腹感中也起作用。目前尚不清楚中枢给予的CCK的饱腹感作用与外周给予的CCK的饱腹感作用有何关系。当前的研究旨在建立一个连贯的神经内分泌机制模式，该模式涉及（从胃肠道壁经大脑到一种动机行为）进餐时摄入的食物导致进餐结束这一事实。
