Mitochondrial uncoupling proteins and energy metabolism.
Mitochondrial uncoupling proteins and energy metabolism.
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DOI：
10.3389/fphys.2015.00036
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发表时间：
2015
影响因子：
4
通讯作者：
Lombardi A
中科院分区：
文献类型：
--
作者：
Busiello RA;Savarese S;Lombardi A
了解促进能量代谢（EM）的代谢因素对于肥胖和相关疾病的新治疗方法的发展至关重要。线粒体氧化磷酸化与ATP合成并不完美耦合，质子泄漏过程起着至关重要的作用。质子泄漏是静息代谢率（RMR）的重要组成部分，因此增强这一过程代表了肥胖治疗的潜在目标。自从发现解偶联蛋白以来，由于它们参与线粒体诱导的质子泄漏，引起了极大的兴趣。解偶联蛋白1 （uncoupling protein 1, UCP1）是该家族中最早被发现的解偶联蛋白1 （uncoupling protein 1, UCP1）具有广泛的解偶联/产热作用，但其同源物UCP3催化的反应及其生理作用仍存在争议。本文综述了UCP1和UCP3在线粒体解偶联/功能以及EM中的作用，并表明它们是治疗肥胖及其相关疾病（如II型糖尿病）的潜在治疗靶点。
Understanding the metabolic factors that contribute to energy metabolism (EM) is critical for the development of new treatments for obesity and related diseases. Mitochondrial oxidative phosphorylation is not perfectly coupled to ATP synthesis, and the process of proton-leak plays a crucial role. Proton-leak accounts for a significant part of the resting metabolic rate (RMR) and therefore enhancement of this process represents a potential target for obesity treatment. Since their discovery, uncoupling proteins have stimulated great interest due to their involvement in mitochondrial-inducible proton-leak. Despite the widely accepted uncoupling/thermogenic effect of uncoupling protein one (UCP1), which was the first in this family to be discovered, the reactions catalyzed by its homolog UCP3 and the physiological role remain under debate. This review provides an overview of the role played by UCP1 and UCP3 in mitochondrial uncoupling/functionality as well as EM and suggests that they are a potential therapeutic target for treating obesity and its related diseases such as type II diabetes mellitus.
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