Ciliary Neurotrophic Factor: a novel theraputic agent for the prevention of muscle insulin resistance

睫状神经营养因子：预防肌肉胰岛素抵抗的新型治疗剂

• 批准号: nhmrc : 392206
• 负责人: Prof Mark Febbraio
• 金额: $ 40.19万
• 依托单位: Baker IDI Heart and Diabetes Institute
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2006
• 资助国家: 澳大利亚
• 起止时间: 2006-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/ciliary-neurotrophic-factor-insulin-resistance/101021
• 关键词: Ciliary; Neurotrophic; Factor; novel; theraputic

In 1995 leptin was discovered and scientists world-wide hoped that this was the great panacea in the treatment of obesity related disorders. Alas, from 1995-1997 the identification of a novel cytokine inducible compound termed suppressor of cytokine signaling (SOCS) that negatively regulated leptin signalling and lead to leptin resistance, quashing hopes for a viable anti-obesogenic drug. Recently, however, work from our group has demonstrated that the neuropoietic cytokine, ciliary neurotrophic factor (CNTF), can act in an anti-obesogenic fashion in a manner similar to leptin. However, unlike leptin, when we place rodents on a high fat diet, the effects of CNTF persist and override induction SOCS proteins. This project will examine the biochemical pathways that allow the actions of CNTF to persist in the presence of diet-induced obesity. This is of major significance because in completing this work, the potential for the development of peripheral tissue drug targets for the treatment of obesity related diseases are both tangible and realistic.

1995年，瘦素被发现，世界各地的科学家希望这是治疗肥胖相关疾病的灵丹妙药。唉，从1995年至1997年，一种新的细胞因子诱导的化合物被称为细胞因子信号转导抑制因子（SOCS）的鉴定，负调节瘦素信号转导，导致瘦素抵抗，粉碎了对一个可行的抗肥胖药物的希望。然而，最近，我们小组的工作表明，神经细胞因子，睫状神经营养因子（CNTF），可以在抗肥胖的方式类似于瘦素。然而，与瘦素不同的是，当我们将啮齿动物置于高脂肪饮食中时，CNTF的作用持续存在并覆盖SOCS蛋白的诱导。该项目将研究允许CNTF的作用在饮食诱导的肥胖存在的情况下持续存在的生化途径。这具有重要意义，因为在完成这项工作时，开发用于治疗肥胖相关疾病的外周组织药物靶点的潜力是有形的和现实的。