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Mitochondrial regulation of insulin action.

机译:线粒体对胰岛素作用的调节。

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摘要

Insulin resistance is the prodrome of many metabolic diseases and identifying ways to correct this pathological condition is a major goal for medical research. The foremost barrier to the development of new treatments is that the precise etiology of insulin resistance is uncertain. Recent studies suggest that changes in mitochondrial structure or function drive this condition, however much of this evidence is circumstantial. This Signaling Networks in Focus article provides a brief overview of known and speculative regulatory intersections whereby mitochondrial dysfunction at the levels of lipid oxidation, oxidative stress, calcium, adenine nucleotides, and protons may regulate insulin sensitivity. If mitochondrial dysfunction underlies the origins of metabolic disease then determining the precise molecular pathway will be essential for the development of new treatment and prevention strategies.
机译:胰岛素抵抗是许多新陈代谢疾病的症结所在,确定纠正这种病理状况的方法是医学研究的主要目标。开发新疗法的最大障碍是胰岛素抵抗的确切病因尚不确定。最近的研究表明,线粒体结构或功能的改变驱动了这种情况,然而,许多证据是间接的。这篇“重点关注的信号网络”文章简要概述了已知的和推测性的调控交叉点,据此,线粒体功能障碍在脂质氧化,氧化应激,钙,腺嘌呤核苷酸和质子水平上可能会调节胰岛素敏感性。如果线粒体功能障碍是代谢疾病起源的基础,那么确定精确的分子途径对于开发新的治疗和预防策略至关重要。

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