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关于右芬氟拉明的作用机制:对瘦人和肥胖者的异食症及食欲动机的影响。

On the mechanism of action of dexfenfluramine: effect on alliesthesia and appetite motivation in lean and obese subjects.

作者信息

Blundell J E, Hill A J

机构信息

Psychology Department, University of Leeds, U.K.

出版信息

Clin Neuropharmacol. 1988;11 Suppl 1:S121-34.

PMID:3180107
Abstract

This study investigated the intensity of two phenomena--perceived pleasantness of sweet tasting solutions, and subjective motivations related to eating--in lean and obese subjects. The study also examined the way in which dexfenfluramine influenced these phenomena as the basis of a mechanism underlying the action of dexfenfluramine on satiation. Such investigations had not previously been carried out on obese people. In lean subjects, glucose-induced negative gustative alliesthesia (NGA) was present but was not affected by drug administration. Dexfenfluramine did, however, markedly influence motivational ratings and subsequent food consumption in a test meal. In obese subjects, NGA was not present nor was it instated by drug treatment. Motivational ratings were strongly influenced by dexfenfluramine. Although hunger ratings were very low in obese subjects, they were further suppressed by the glucose load and by the drug. Hunger suppression was greater in obese than lean subjects. These results suggest that a decline in the pleasantness of a sweet taste is not a mechanism through which fenfluramine exerts an anorectic action. The data suggest that the suppression of subjective motivation to eat is implicated in the reduction of food intake by dexfenfluramine in lean subjects, and in the weight loss observed in obese people.

摘要

本研究调查了瘦人和肥胖受试者中两种现象的强度——甜味溶液的感知愉悦度以及与进食相关的主观动机。该研究还考察了右芬氟拉明影响这些现象的方式,以此作为右芬氟拉明对饱腹感作用机制的基础。此前尚未对肥胖人群进行过此类研究。在瘦人受试者中,存在葡萄糖诱导的负性味觉变适(NGA),但不受药物给药的影响。然而,右芬氟拉明在试餐中确实显著影响了动机评分以及随后的食物摄入量。在肥胖受试者中,不存在NGA,药物治疗也未使其产生。动机评分受到右芬氟拉明的强烈影响。尽管肥胖受试者的饥饿评分非常低,但葡萄糖负荷和药物进一步抑制了饥饿感。肥胖受试者的饥饿抑制程度大于瘦人受试者。这些结果表明,甜味愉悦度的下降并非芬氟拉明发挥厌食作用的机制。数据表明,抑制主观进食动机与右芬氟拉明减少瘦人受试者的食物摄入量以及肥胖者体重减轻有关。

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Clin Neuropharmacol. 1988;11 Suppl 1:S121-34.
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