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首页> 外文期刊>Cell metabolism >Hepatic-specific disruption of SIRT6 in mice results in fatty liver formation due to enhanced glycolysis and triglyceride synthesis.
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Hepatic-specific disruption of SIRT6 in mice results in fatty liver formation due to enhanced glycolysis and triglyceride synthesis.

机译：由于增强的糖酵解和甘油三酸酯合成，小鼠中SIRT6的肝特异性破坏导致脂肪肝形成。

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Under various conditions, mammals have the ability to maintain serum glucose concentration within a narrow range. SIRT1 plays an important role in regulating gluconeogenesis and fat metabolism; however, the underlying mechanisms remain elusive. Here, we show that SIRT1 forms a complex with FOXO3a and NRF1 on the SIRT6 promoter and positively regulates expression of SIRT6, which, in turn, negatively regulates glycolysis, triglyceride synthesis, and fat metabolism by deacetylating histone H3 lysine 9 in the promoter of many genes involved in these processes. Liver-specific deletion of SIRT6 in mice causes profound alterations in gene expression, leading to increased glycolysis, triglyceride synthesis, reduced beta oxidation, and fatty liver formation. Human fatty liver samples exhibited significantly lower levels of SIRT6 than did normal controls. Thus, SIRT6 plays a critical role in fat metabolism and may serve as a therapeutic target for treating fatty liver disease, the most common cause of liver dysfunction in humans.
机译：在各种条件下，哺乳动物具有将血清葡萄糖浓度维持在狭窄范围内的能力。 SIRT1在调节糖异生和脂肪代谢中起重要作用。但是，基本机制仍然难以捉摸。在这里，我们显示SIRT1在SIRT6启动子上与FOXO3a和NRF1形成复合物，并正向调节SIRT6的表达，而SIRT6则通过在许多启动子中使组蛋白H3赖氨酸9脱乙酰化而负向调节糖酵解，甘油三酸酯合成和脂肪代谢。这些过程中涉及的基因。小鼠中SIRT6的肝脏特异性缺失导致基因表达发生深刻变化，从而导致糖酵解增加，甘油三酸酯合成增加，β氧化减少和脂肪肝形成。人脂肪肝样品的SIRT6水平明显低于正常对照。因此，SIRT6在脂肪代谢中起关键作用，并且可以作为治疗脂肪肝疾病的治疗靶点，而脂肪肝疾病是人类最常见的肝功能异常的原因。

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