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首页> 外文期刊>Cell metabolism >Cardiolipin remodeling by ALCAT1 links oxidative stress and mitochondrial dysfunction to obesity.
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Cardiolipin remodeling by ALCAT1 links oxidative stress and mitochondrial dysfunction to obesity.

机译：通过ALCAT1进行的心磷脂重塑将氧化应激和线粒体功能障碍与肥胖联系起来。

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摘要

Oxidative stress causes mitochondrial dysfunction and metabolic complications through unknown mechanisms. Cardiolipin (CL) is a key mitochondrial phospholipid required for oxidative phosphorylation. Oxidative damage to CL from pathological remodeling is implicated in the etiology of mitochondrial dysfunction commonly associated with diabetes, obesity, and other metabolic diseases. Here, we show that ALCAT1, a lyso-CL acyltransferase upregulated by oxidative stress and diet-induced obesity (DIO), catalyzes the synthesis of CL species that are highly sensitive to oxidative damage, leading to mitochondrial dysfunction, ROS production, and insulin resistance. These metabolic disorders were reminiscent of those observed in type 2 diabetes and were reversed by rosiglitazone treatment. Consequently, ALCAT1 deficiency prevented the onset of DIO and significantly improved mitochondrial complex I activity, lipid oxidation, and insulin signaling in ALCAT1(-/-) mice. Collectively, these findings identify a key role of ALCAT1 in regulating CL remodeling, mitochondrial dysfunction, and susceptibility to DIO.
机译：氧化应激通过未知机制导致线粒体功能障碍和代谢并发症。心磷脂（CL）是氧化磷酸化所需的关键线粒体磷脂。病理重塑对CL的氧化损伤与通常与糖尿病，肥胖症和其他代谢性疾病有关的线粒体功能障碍的病因有关。在这里，我们表明，ALCAT1是一种被氧化应激和饮食诱发的肥胖（DIO）上调的溶酶-CL酰基转移酶，可催化对氧化损伤高度敏感的CL物质的合成，从而导致线粒体功能障碍，ROS产生和胰岛素抵抗。这些代谢异常使人联想到在2型糖尿病中观察到的代谢异常，并通过罗格列酮治疗得以逆转。因此，ALCAT1缺乏症阻止了DIO的发作，并显着改善了ALCAT1（-/-）小鼠的线粒体I活性，脂质氧化和胰岛素信号传导。总而言之，这些发现确定了ALCAT1在调节CL重塑，线粒体功能障碍和对DIO的敏感性中的关键作用。

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