Yim G K, Lowy M T
Fed Proc. 1984 Nov;43(14):2893-7.
This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.
本综述总结了近期聚焦于内源性阿片类物质（EOs）和阿片受体在食物摄入控制中作用的研究工作。尽管阿片拮抗剂的厌食作用如今已被广泛接受，但其确切的内源性阿片类物质、作用位点及作用机制仍有待确定。然而，越来越多的证据表明，强啡肽（一种κ型阿片受体的内源性配体）是食欲的重要调节因子（刺激物）。其他内源性阿片类物质，如β-内啡肽的作用则不太明确。内源性阿片类物质似乎参与维持正常的进食行为，并且可能是导致遗传性肥胖和应激个体脂肪过度消耗的原因。阿片拮抗剂可阻止美味食物的过度摄入，因此为一些超重个体提供了一种有前景的减肥方法。厌食可能源于κ型阿片活性的缺乏，令人惊讶的是，也可能由阿片活性过高导致。事实上，μ型阿片拮抗剂（纳洛酮）在某些厌食情况下可增加进食量和体重。因此，似乎阿片激动剂活性过高可能导致食欲亢进或厌食（取决于阿片受体类型）。最后，阿片拮抗剂可能有助于使这两种病理性进食状态恢复正常。
