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甘丙肽样肽通过自主神经系统介导对肝脏和脂肪组织脂质代谢的影响。

Autonomic nervous system-mediated effects of galanin-like peptide on lipid metabolism in liver and adipose tissue.

作者信息

Hirako Satoshi, Wada Nobuhiro, Kageyama Haruaki, Takenoya Fumiko, Izumida Yoshihiko, Kim Hyounju, Iizuka Yuzuru, Matsumoto Akiyo, Okabe Mai, Kimura Ai, Suzuki Mamiko, Yamanaka Satoru, Shioda Seiji

机构信息

Department of Health and Nutrition, University of Human Arts and Sciences, Saitama, Japan.

Department of Internal Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

出版信息

Sci Rep. 2016 Feb 19;6:21481. doi: 10.1038/srep21481.

Abstract

Galanin-like peptide (GALP) is a neuropeptide involved in the regulation of feeding behavior and energy metabolism in mammals. While a weight loss effect of GALP has been reported, its effects on lipid metabolism have not been investigated. The aim of this study was to determine if GALP regulates lipid metabolism in liver and adipose tissue via an action on the sympathetic nervous system. The respiratory exchange ratio of mice administered GALP intracerebroventricularly was lower than that of saline-treated animals, and fatty acid oxidation-related gene mRNA levels were increased in the liver. Even though the respiratory exchange ratio was reduced by GALP, this change was not significant when mice were treated with the sympatholytic drug, guanethidine. Lipolysis-related gene mRNA levels were increased in the adipose tissue of GALP-treated mice compared with saline-treated animals. These results show that GALP stimulates fatty acid β-oxidation in liver and lipolysis in adipose tissue, and suggest that the anti-obesity effect of GALP may be due to anorexigenic actions and improvement of lipid metabolism in peripheral tissues via the sympathetic nervous system.

摘要

甘丙肽样肽(GALP)是一种神经肽,参与哺乳动物进食行为和能量代谢的调节。虽然已有报道称GALP具有减肥作用,但其对脂质代谢的影响尚未得到研究。本研究的目的是确定GALP是否通过作用于交感神经系统来调节肝脏和脂肪组织中的脂质代谢。脑室内注射GALP的小鼠的呼吸交换率低于生理盐水处理的动物,并且肝脏中脂肪酸氧化相关基因的mRNA水平升高。尽管GALP降低了呼吸交换率,但在用交感神经阻滞剂胍乙啶处理小鼠时,这种变化并不显著。与生理盐水处理的动物相比,GALP处理的小鼠脂肪组织中脂解相关基因的mRNA水平升高。这些结果表明,GALP刺激肝脏中的脂肪酸β-氧化和脂肪组织中的脂解,并表明GALP的抗肥胖作用可能归因于通过交感神经系统产生的厌食作用和外周组织脂质代谢的改善。

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