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巯基乙酸钠诱导的脂肪缺乏性喂养的药理学拮抗作用。

Pharmacological antagonism of lipoprivic feeding induced by sodium mercaptoacetate.

作者信息

Garosi V L, Nisoli E, Blundell J E, Carruba M O

机构信息

Section of Pharmacology, Toxicology, and Experimental Therapeutics, School of Medicine, University of Brescia, Italy.

出版信息

Eur J Pharmacol. 1995 Apr 4;276(3):285-9. doi: 10.1016/0014-2999(95)00087-2.

Abstract

Drugs, such as sodium mercaptoacetate and methylpalmoxirate, which block fatty acid oxidation at different levels in the metabolic pathway, stimulate feeding. It is well known that selective centrally induced stimulation of dopamine, serotonin (5-hydroxytryptamine, 5-HT) and beta-adrenoceptors, or inhibition of the opiatergic system substantially decrease food intake in rats trained to eat 4 h a day. The results of the present study show that centrally acting dopaminergic and serotoninergic anorectic drugs, the opiate receptor antagonist naloxone, the alpha-adrenoceptor blocking drug phentolamine, and peripherally administered 5-HT counteract the overeating induced by mercaptoacetate. Comparing these effects to those described in 2-deoxy-D-glucose- and insulin-induced feeding, our data support the proposition that distinct neural circuits are involved in the hyperphagic responses to diverse metabolic stimuli.

摘要

诸如巯基乙酸钠和甲基棕榈酰肉碱等药物,它们在代谢途径的不同水平阻断脂肪酸氧化,会刺激进食。众所周知,选择性地在中枢诱导多巴胺、5-羟色胺(5-羟色胺,5-HT)和β-肾上腺素能受体的刺激,或抑制阿片能系统,会使每天训练进食4小时的大鼠的食物摄入量大幅减少。本研究结果表明,中枢作用的多巴胺能和5-羟色胺能厌食药物、阿片受体拮抗剂纳洛酮、α-肾上腺素能阻断药物酚妥拉明以及外周给予的5-羟色胺可抵消巯基乙酸盐诱导的暴饮暴食。将这些作用与2-脱氧-D-葡萄糖和胰岛素诱导的进食中所描述的作用进行比较,我们的数据支持这样一种观点,即不同的神经回路参与了对多种代谢刺激的贪食反应。

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