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在存在δ阿片受体拮抗剂ICI 174,864的情况下,2-脱氧-D-葡萄糖诱导的摄食过量。

Hyperphagia induced by 2-deoxy-D-glucose in the presence of the delta-opioid antagonist ICI 174,864.

作者信息

Jackson H C, Sewell R D

出版信息

Neuropharmacology. 1985 Aug;24(8):815-7. doi: 10.1016/0028-3908(85)90018-8.

Abstract

The effect of the selective delta-opioid antagonist ICI 174,864 (N,N-bisallyl-Tyr-Aib-Aib-Phe-Leu-OH: Aib=alpha-aminoisobutyric acid) on the hyperphagia induced by 2-deoxy-D-glucose (2-DG) was investigated in non-deprived rats. The increase in food intake produced by 2-DG (500 mg/kg i.p.) was not reduced by ICI 174,864 at a dose (3 micrograms/rat i.c.v.) which totally abolished the feeding response to the delta-agonist D-Ala2-D-Leu5-enkephalin (10 micrograms/rat i.c.v.). These findings suggest that the appetitive effects of 2-DG are not mediated by an enkephalinergic/delta-receptor system. They do not, however, preclude the possible involvement of endogenous opioids acting at other sub-types of opioid receptor in this glucoprivic ingestional response, which is suppressed by less specific opioid antagonists such as naloxone.

摘要

在未禁食的大鼠中研究了选择性δ-阿片受体拮抗剂ICI 174,864(N,N-双烯丙基-Tyr-Aib-Aib-Phe-Leu-OH:Aib =α-氨基异丁酸)对2-脱氧-D-葡萄糖(2-DG)诱导的摄食亢进的影响。2-DG(500mg / kg腹腔注射)引起的食物摄入量增加,并未被ICI 174,864(3μg/大鼠脑室内注射)降低,该剂量可完全消除对δ-激动剂D-Ala2-D-Leu5-脑啡肽(10μg/大鼠脑室内注射)的摄食反应。这些发现表明,2-DG的食欲作用不是由脑啡肽能/δ-受体系统介导的。然而,它们并不排除内源性阿片类物质可能作用于其他类型阿片受体参与这种糖缺乏性摄食反应,这种反应可被纳洛酮等特异性较低的阿片受体拮抗剂抑制。

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