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内源性阿片肽β-内啡肽在能量平衡中的作用。

A role for the endogenous opioid beta-endorphin in energy homeostasis.

作者信息

Appleyard Suzanne M, Hayward Michael, Young Juan I, Butler Andrew A, Cone Roger D, Rubinstein Marcelo, Low Malcolm J

机构信息

Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.

出版信息

Endocrinology. 2003 May;144(5):1753-60. doi: 10.1210/en.2002-221096.

Abstract

Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and beta-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack beta-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, beta-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to beta-endorphin that physiologically stimulates feeding. These genetic data indicate that beta-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of beta-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis.

摘要

下丘脑的促阿黑皮素原(POMC)神经元是脂肪稳态激素瘦素的直接作用靶点,通过整合外周和中枢信息来维持能量平衡。促黑素细胞激素和β-内啡肽神经肽由POMC加工而来,并可能在轴突终末共同释放。药理学和遗传学方法相结合的研究表明,促黑素细胞激素对食欲和体重有抑制作用。相比之下,药理学研究通常表明阿片类物质会刺激食物摄入。在此我们报告,经过基因工程改造后选择性缺乏β-内啡肽但保留正常促黑素细胞激素信号传导的雄性小鼠出现食欲亢进和肥胖。此外,β-内啡肽突变小鼠和野生型小鼠对外源性阿片类物质具有相同的促食欲反应,对非选择性阿片类拮抗剂纳洛酮具有相同的抑食欲反应,这意味着存在一种替代β-内啡肽的内源性阿片类物质基调,在生理上刺激进食。这些遗传学数据表明,β-内啡肽是正常进食调节所必需的,但与早期关于β-内啡肽和促黑素细胞激素对食欲有相反作用的报道不同,我们的结果表明,内源性释放的POMC衍生肽在能量平衡调节中存在更具互补性的相互作用。

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