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首页> 外文期刊>Cell metabolism >Disruption of Acetyl-Lysine Turnover in Muscle Mitochondria Promotes Insulin Resistance and Redox Stress without Overt Respiratory Dysfunction
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Disruption of Acetyl-Lysine Turnover in Muscle Mitochondria Promotes Insulin Resistance and Redox Stress without Overt Respiratory Dysfunction

机译：肌肉线粒体中乙酰赖氨酸周转的破坏促进胰岛素抵抗和氧化还原胁迫而没有明显呼吸功能障碍

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摘要

This study sought to examine the functional significance of mitochondria! protein acetylation using a double knockout (DKO) mouse model harboring muscle-specific deficits in acetyl-CoA buffering and lysine deacetylation, due to genetic ablation of carnitine acetyltransferase and Sirtuin 3, respectively. DKO mice are highly susceptible to extreme hyperacetylation of the mitochondrial proteome and develop a more severe form of diet-induced insulin resistance than either single KO mouse line. However, the functional phenotype of hyperacetylated DKO mitochondria is largely normal. Of the >120 measures of respiratory function assayed, the most consistently observed traits of a markedly heightened acetyl-lysine landscape are enhanced oxygen flux in the context of fatty acid fuel and elevated rates of electron leak. In sum, the findings challenge the notion that lysine acetylation causes broad-ranging damage to mitochondria! quality and performance and raise the possibility that acetyl-lysine turnover, rather than acetyl-lysine stoichiometry, modulates redox balance and carbon flux.
机译：该研究寻求研究线粒体的功能意义！由于肉碱乙酰转移酶和Sirtuin 3的遗传消融，使用双敲除（DKO）小鼠模型含有双敲除（DKO）小鼠模型的双敲除（DKO）小鼠模型，含有氨基酰乙酰转移酶和Sirtuin 3的遗传烧蚀。 DKO小鼠对线粒体蛋白质组的极端缩小化学化高度敏感，并且产生比单一KO小鼠线的更严重的饮食诱导的胰岛素抵抗形式。然而，过乙酰化DKO线粒体的功能表型在很大程度上是正常的。在测定脂肪酸燃料的背景下显着提高的乙酰赖氨酸景观的最常见的乙酰赖氨酸景观的氧气通量和电子泄漏率升高的乙酰赖氨酸景观中最常见的乙酰赖氨酸景观的性状。总而言之，调查结果挑战赖氨酸乙酰化导致对线粒体造成广泛损伤的观念！质量和性能，提高乙酰赖氨酸周转，而不是乙酰赖氨酸化学计量，调节氧化还原平衡和碳通量。

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