μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals
μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals
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DOI：
10.1152/ajpregu.00406.2010
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发表时间：
2011-07-01
影响因子：
2.8
通讯作者：
Taha, Sharif A.
中科院分区：
文献类型：
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作者：
Katsuura, Yoshihiro;Heckmann, Jennifer A.;Taha, Sharif A.
Katsuura Y，Heckmann JA，Taha SA.丘脑核中的μ-阿片受体刺激通过增加适口性和抑制饱足感信号来提高促脂剂摄入。Am J Physiol Regul Integr Comp Physiol 301：R244-R254，2011。首次发表于2011年5月4日; doi：10.1152/ajpregu.00406.2010.-将μ-阿片受体（莫尔）激动剂输注到丘脑核（NAcc）中驱动贪婪的食物摄入，这是一种假设通过增加促味剂适口性而发生的效应。虽然莫尔刺激可提高许多可口食物的摄入量，但这种操纵对脂肪食物摄入具有优先效应。即使在基线条件下偏好富含碳水化合物的替代品的大鼠中，NAcc莫尔刺激也会增加高脂肪食物的消耗。这表明NAcc莫尔刺激可能不仅仅增强适口性信号，并提高了介导脂肪摄入的机制可能不同于其他促味剂摄入的机制的可能性。本研究旨在探讨NAcc莫尔刺激对脂肪食物摄入影响的生理机制。在实验1中，我们分析了舔微结构在大鼠ingredient Intraperoid，以确定潜在的喂养诱导的MOR特异性激动剂注入NAcc的变化。NAcc核心而非外壳中的莫尔刺激增加了爆发持续时间和第一分钟舔，同时增加了Intraperoid摄入的速率和持续时间。这些结果表明，核心中的莫尔激活增加了内脏的适口性并减弱了抑制性摄食后反馈。在实验2中，我们测量了NAcc核心中的莫尔刺激对非营养性olestra消耗的影响。MOR-特异性激动剂剂量依赖性地增加了olestra摄入，表明热量信号传导对于由NAcc莫尔刺激诱导的摄食过多不是必需的。在实验1和2中由药物输注诱导的摄食被莫尔拮抗剂阻断。在实验3中，我们确定了NAcc核心中的莫尔激活是否可以减弱由将黑皮质素激动剂MTII输注到第三脑室中引起的饱腹感相关信号传导。莫尔刺激可逆转MTII引起的摄食抑制。总之，我们的研究结果表明，莫尔刺激NAcc核心通过依赖于orosensory线索的适口性机制和抑制饱腹感信号抑制食物摄入来提高脂肪食物摄入。
Katsuura Y, Heckmann JA, Taha SA. mu-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals. Am J Physiol Regul Integr Comp Physiol 301: R244-R254, 2011. First published May 4, 2011; doi:10.1152/ajpregu.00406.2010.-Infusion of a mu-opioid receptor (MOR) agonist into the nucleus accumbens (NAcc) drives voracious food intake, an effect hypothesized to occur through increased tastant palatability. While intake of many palatable foods is elevated by MOR stimulation, this manipulation has a preferential effect on fatty food ingestion. Consumption of high-fat foods is increased by NAcc MOR stimulation even in rats that prefer a carbohydrate-rich alternative under baseline conditions. This suggests that NAcc MOR stimulation may not simply potentiate palatability signals and raises the possibility that mechanisms mediating fat intake may be distinct from those underlying intake of other tastants. The present study was conducted to investigate the physiological mechanisms underlying the effects of NAcc MOR stimulation on fatty food intake. In experiment 1, we analyzed lick microstructure in rats ingesting Intralipid to identify the changes underlying feeding induced by infusion of a MOR-specific agonist into the NAcc. MOR stimulation in the NAcc core, but not shell, increased burst duration and first-minute licks, while simultaneously increasing the rate and duration of Intralipid ingestion. These results suggest that MOR activation in the core increases Intralipid palatability and attenuates inhibitory postingestive feedback. In experiment 2, we measured the effects of MOR stimulation in the NAcc core on consumption of nonnutritive olestra. A MOR-specific agonist dose dependently increased olestra intake, demonstrating that caloric signaling is not required for hyperphagia induced by NAcc MOR stimulation. Feeding induced by drug infusion in both experiments 1 and 2 was blocked by a MOR antagonist. In experiment 3, we determined whether MOR activation in the NAcc core could attenuate satiety-related signaling caused by infusion of the melanocortin agonist MTII into the third ventricle. Suppression of intake caused by MTII was reversed by MOR stimulation. Together, our results suggest that MOR stimulation in the NAcc core elevates fatty food intake through palatability mechanisms dependent on orosensory cues and suppression of satiety signals inhibiting food intake.