Paraventricular nucleus anandamide signaling alters eating and substrate oxidation
Paraventricular nucleus anandamide signaling alters eating and substrate oxidation
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DOI：
10.1097/wnr.0b013e32835271d1
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发表时间：
2012-05-09
期刊：
影响因子：
1.7
通讯作者：
Currie, Paul J.
中科院分区：
文献类型：
--
作者：
Chapman, Colin D.;Dono, Lindsey M.;Currie, Paul J.
在中枢神经系统中，内源性大麻素anandamide [n-花生四烯酰基乙醇胺（AEA）]被认为通过按需激活下丘脑回路来增加食物摄入量。本研究研究了下丘脑室旁核（PVN）注射AEA （25-400 pmol）对食物摄入和能量底物氧化[呼吸商（RQ）]的影响。PVN给药增加了进食行为和RQ，表明碳水化合物氧化增强。此外，PVN给药大麻素1型受体逆激动剂AM251 （5-10 μ g）减弱了AEA （100 pmol）引起的进食和RQ反应。单独服用AM251不会改变食物摄入量或RQ。总的来说，这些发现与PVN大麻素1型受体在调节饮食和能量稳态中的作用是一致的。神经报告23:425-429 (C) 2012 Wolters Kluwer Health垂直bar Lippincott Williams & Wilkins。
In the central nervous system, the endocannabinoid anandamide [N-arachidonoylethanolamine (AEA)] is believed to increase food intake through on-demand activation of hypothalamic circuits. The present study examined the effects of hypothalamic paraventricular nucleus (PVN) injections of AEA (25-400 pmol) on food intake and energy substrate oxidation [respiratory quotient (RQ)]. PVN administration of AEA increased eating behavior and RQ, indicating enhanced carbohydrate oxidation. Further, PVN administration of the cannabinoid type 1 receptor inverse agonist AM251 (5-10 mu g) attenuated both the eating and the RQ responses elicited by AEA (100 pmol). AM251 administered alone did not alter food intake or RQ. Overall, these findings are consistent with a role for PVN cannabinoid type 1 receptors in the regulation of eating and energy homeostasis. NeuroReport 23: 425-429 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.