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gp130受体配体作为肥胖症的潜在治疗靶点。

gp130 receptor ligands as potential therapeutic targets for obesity.

作者信息

Febbraio Mark A

机构信息

Cellular and Molecular Metabolism Laboratory, Division of Diabetes and Metabolism, Baker Heart Research Institute, Melbourne, Victoria, Australia.

出版信息

J Clin Invest. 2007 Apr;117(4):841-9. doi: 10.1172/JCI30453.

DOI:10.1172/JCI30453
PMID:17404609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1838942/
Abstract

Obesity and its related cluster of pathophysiologic conditions including insulin resistance, glucose intolerance, dyslipidemia, and hypertension are recognized as growing threats to world health. It is now estimated that 10% of the world's population is overweight or obese. As a result, new therapeutic options for the treatment of obesity are clearly warranted. Recent research has focused on the role that gp130 receptor ligands may play as potential therapeutic targets in obesity. One cytokine in particular, ciliary neurotrophic factor (CNTF), acts both centrally and peripherally and mimics the biologic actions of the appetite control hormone leptin, but unlike leptin, CNTF appears to be effective in obesity and as such may have therapeutic potential. In addition, CNTF suppresses inflammatory signaling cascades associated with lipid accumulation in liver and skeletal muscle. This review examines the potential role of gp130 receptor ligands as part of a therapeutic strategy to treat obesity.

摘要

肥胖及其相关的一系列病理生理状况,包括胰岛素抵抗、葡萄糖不耐受、血脂异常和高血压,被认为是对全球健康日益增长的威胁。据估计,目前全球10%的人口超重或肥胖。因此,显然需要新的肥胖治疗选择。最近的研究集中在gp130受体配体作为肥胖潜在治疗靶点可能发挥的作用。特别是一种细胞因子,睫状神经营养因子(CNTF),它在中枢和外周均有作用,可模拟食欲控制激素瘦素的生物学作用,但与瘦素不同的是,CNTF在肥胖治疗中似乎有效,因此可能具有治疗潜力。此外,CNTF可抑制与肝脏和骨骼肌脂质积累相关的炎症信号级联反应。本综述探讨了gp130受体配体作为肥胖治疗策略一部分的潜在作用。

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gp130 receptor ligands as potential therapeutic targets for obesity.gp130受体配体作为肥胖症的潜在治疗靶点。
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2
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本文引用的文献

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AMP-activated protein kinase-regulated activation of the PGC-1alpha promoter in skeletal muscle cells.骨骼肌细胞中AMP激活的蛋白激酶调节的PGC-1α启动子激活
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gp130 signaling in proopiomelanocortin neurons mediates the acute anorectic response to centrally applied ciliary neurotrophic factor.促阿片黑素皮质素原神经元中的gp130信号传导介导了对中枢给予睫状神经营养因子的急性厌食反应。
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Ciliary neurotrophic factor suppresses hypothalamic AMP-kinase signaling in leptin-resistant obese mice.睫状神经营养因子抑制瘦素抵抗性肥胖小鼠下丘脑的AMP激酶信号传导。
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