线粒体脂肪酸合成是哺乳动物氧化代谢的一个新兴中心调节因子。

Cell metabolism Pub Date : 2024-01-02 Epub Date: 2023-12-20 DOI:10.1016/j.cmet.2023.11.017
Riley J Wedan, Jacob Z Longenecker, Sara M Nowinski
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引用次数: 0

摘要

与众所周知的营养物质分解功能相反,线粒体也是重要的生物合成枢纽,并表达进化保守的线粒体脂肪酸合成(mtFAS)途径。mtFAS 生成硫辛酸和更长的饱和脂肪酸,但其确切产物、在细胞中的最终目的地以及该途径的细胞意义都是目前研究的热点问题。此外,尽管线粒体具有明确的输入脂肪酸的能力,但为什么线粒体需要 mtFAS,目前仍不清楚。mtFAS 基因先天性代谢错误患者的发现引发了对该途径的新的研究兴趣。新的哺乳动物模型揭示了 mtFAS 如何协调线粒体氧化代谢的许多方面,并提出了它在肥胖、糖尿病和心力衰竭等疾病中的作用问题。在这篇综述中,我们将讨论 mtFAS 的产物、它们的功能以及 mtFAS 在各种模型和代谢性疾病中受损的后果。
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Mitochondrial fatty acid synthesis is an emergent central regulator of mammalian oxidative metabolism.

Contrary to their well-known functions in nutrient breakdown, mitochondria are also important biosynthetic hubs and express an evolutionarily conserved mitochondrial fatty acid synthesis (mtFAS) pathway. mtFAS builds lipoic acid and longer saturated fatty acids, but its exact products, their ultimate destination in cells, and the cellular significance of the pathway are all active research questions. Moreover, why mitochondria need mtFAS despite their well-defined ability to import fatty acids is still unclear. The identification of patients with inborn errors of metabolism in mtFAS genes has sparked fresh research interest in the pathway. New mammalian models have provided insights into how mtFAS coordinates many aspects of oxidative mitochondrial metabolism and raise questions about its role in diseases such as obesity, diabetes, and heart failure. In this review, we discuss the products of mtFAS, their function, and the consequences of mtFAS impairment across models and in metabolic disease.

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