Chapman Colin D, Dono Lindsey M, French Matthew C, Weinberg Zachary Y, Schuette Lindsey M, Currie Paul J
Department of Psychology, Reed College, 3203 SE Woodstock Blvd, Portland, Oregon 97202, USA.
Neuroreport. 2012 May 9;23(7):425-9. doi: 10.1097/WNR.0b013e32835271d1.
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 μg) 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.
在中枢神经系统中，内源性大麻素花生四烯酸乙醇胺[N-花生四烯酰乙醇胺（AEA）]被认为通过按需激活下丘脑回路来增加食物摄入量。本研究检测了向下丘脑室旁核（PVN）注射AEA（25 - 400皮摩尔）对食物摄入量和能量底物氧化[呼吸商（RQ）]的影响。向PVN注射AEA会增加进食行为和RQ，表明碳水化合物氧化增强。此外，向PVN注射1型大麻素受体反向激动剂AM251（5 - 10微克）可减弱AEA（100皮摩尔）引发的进食和RQ反应。单独注射AM251不会改变食物摄入量或RQ。总体而言，这些发现与PVN 1型大麻素受体在进食和能量稳态调节中的作用一致。
