Cooper S J, Jackson A, Kirkham T C
Pharmacol Biochem Behav. 1985 Nov;23(5):889-901. doi: 10.1016/0091-3057(85)90088-7.
Evidence from studies which utilise either opiate receptor agonists and antagonists strongly indicate a role for endorphinergic mechanisms in the control of feeding responses. Two means by which these compounds may exert an effect on feeding can be singled-out. Firstly, emerging evidence suggests that the process of achieving satiety (terminating a meal, or choice of a commodity) may be accelerated following treatments with opiate receptor antagonists. Secondly, the preference for highly palatable solutions (sweet solutions have received most attention) in two-bottle tests is blocked after injection of opiate receptor antagonists. This finding has been interpreted in terms of the abolition of the reward or incentive quality associated with the particularly attractive flavour. These two mechanisms of action may represent two aspects of a single, fundamental process. Following an introduction to rat urination model of in vivo kappa agonist activity, the consistent effect of several kappa agonists (including the highly selective U-50,488H) to stimulate food consumption is described. Recognising that members of the dynorphin group of endogenous opioid peptides are kappa receptor ligands, some with a high degree of selectivity, and the evidence the dynorphins and neo-endorphins produce hyperphagia in rats is particularly interesting. Such lines of evidence lead to the hypothesis that peptides of the dynorphin group may act endogenously to promote the expression of normal feeding behaviour.
使用阿片受体激动剂和拮抗剂的研究证据有力地表明，内啡肽能机制在控制进食反应中发挥作用。这些化合物可能影响进食的两种方式可以被明确指出。首先，新出现的证据表明，用阿片受体拮抗剂治疗后，实现饱腹感（结束一餐或选择商品）的过程可能会加速。其次，在双瓶测试中，注射阿片受体拮抗剂后，对高度可口溶液（甜味溶液受到的关注最多）的偏好会被阻断。这一发现被解释为与特别诱人的味道相关的奖励或激励性质的消除。这两种作用机制可能代表了一个单一基本过程的两个方面。在介绍了体内κ激动剂活性的大鼠排尿模型后，描述了几种κ激动剂（包括高度选择性的U-50,488H）刺激食物消耗的一致效果。认识到内源性阿片肽强啡肽组的成员是κ受体配体，其中一些具有高度选择性，并且强啡肽和新内啡肽在大鼠中产生食欲亢进的证据特别有趣。这些证据线索导致这样的假设，即强啡肽组的肽可能在体内起作用以促进正常进食行为的表达。
