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首页> 外文期刊>Journal of Molecular Biology >Protein Lysine Acetylation: Grease or Sand in the Gears of beta-Cell Mitochondria?
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Protein Lysine Acetylation: Grease or Sand in the Gears of beta-Cell Mitochondria?

机译：蛋白质赖氨酸乙酰化：β-细胞线粒体齿轮的润滑脂或砂？

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摘要

Mitochondria carry out many essential functions in metabolism. A central task is the oxidation of nutrients and the generation of ATP by oxidative phosphorylation. Mitochondrial metabolism needs to be tightly regulated for the cell to respond to changes in ATP demand and nutrient supply. Here, we review how protein lysine acetylation contributes to the regulation of mitochondrial metabolism in insulin target tissues and the insulin-secreting pancreatic beta-cell. We summarize recent evidence showing that in pancreatic beta-cells, lysine acetylation occurs on a large number of proteins involved in metabolism. Furthermore, we give a brief overview of the molecular mechanism that controls lysine acetylation dynamics. We propose that protein lysine acetylation is an important mechanism for the fine-tuning of mitochondrial activity in beta-cells during normal physiology. In contrast, nutrient oversupply, oxidative stress, or inhibition of the mitochondrial deacetylase SIRT3 leads to protein lysine hyperacetylation, which impairs mitochondrial function. By perturbing mitochondrial activity in beta-cells and insulin target tissues, protein lysine hyperacetylation may contribute to the development of type 2 diabetes. (C) 2019 Elsevier Ltd. All rights reserved.
机译：线粒体在新陈代谢中开展了许多基本功能。中央任务是氧化磷酸化营养素的氧化和ATP的产生。对于细胞需要紧密调节线粒体代谢，以应对ATP需求和营养供应的变化。在这里，我们审查了蛋白质赖氨酸乙酰化的调节在胰岛素靶组织和胰岛素分泌胰腺β细胞中有助于调节线粒体代谢。我们概述了最近的证据表明，在胰腺β细胞中，赖氨酸乙酰化发生在参与代谢的大量蛋白质上。此外，我们简要概述了控制赖氨酸乙酰化动力学的分子机制。我们提出蛋白质赖氨酸乙酰化是在正常生理过程中β细胞中细胞粒子粒子活性微调的重要机制。相反，营养素供过于求，氧化应激或线粒体脱乙酰酶SIRT3的抑制导致蛋白质赖氨酸过缩酰基化，其损害线粒体功能。通过在β细胞和胰岛素靶组织中扰动线粒体活性，蛋白质赖氨酸过乙酰化可能有助于2型糖尿病的发育。 （c）2019 Elsevier Ltd.保留所有权利。

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