Gut:为什么脂肪会引发脂肪肝

2017-10-16 海北 MedSci原创

肝脏细胞中游离脂肪酸的积累能够诱导脂肪毒性,导致非酒精性脂肪肝的产生。来自浙江大学的研究人员就想通过研究内源性硫化氢(H2S)生物合成的关键酶3-巯基丙酮酸转移酶(MPST)来探索游离脂肪酸引起非酒精性脂肪肝的潜在机制。

肝脏细胞中游离脂肪酸的积累能够诱导脂肪毒性,导致非酒精性脂肪肝的产生。来自浙江大学的研究人员就想通过研究内源性硫化氢(H2S)生物合成的关键酶3-巯基丙酮酸转移酶(MPST)来探索游离脂肪酸引起非酒精性脂肪肝的潜在机制。 研究人员在小鼠和非酒精性脂肪肝患者中进行了MPST表达的研究,并使用多种分子手段研究MPST调节对体内和体外肝脂肪变性的影响。 研究人员发现,在体外利用游离脂肪酸处理肝细胞能够上调MPST的表达,并且该现象是部分依赖于NF-κB/ p65通路的。在高脂肪饮食(HFD)小鼠和非酒精性脂肪肝患者肝脏中,MPST的表达也有显著的增加。利用腺病毒将MPST部分敲低,或是将Mpst基因进行单链敲除都会显著改善高脂肪饮食喂养的小鼠的肝脏脂肪变性情况。一致的是,在L02细胞中进行MPST的抑制也能够降低游离脂肪酸引起的脂肪聚积。 有趣的是,MPST的抑制能够显著增强而不是降低H2S产生,而MPST过表达显著抑制H2S的产生。免疫共沉淀实验表明,MPST与胱硫醚γ-裂解酶(CSE)直接相互作用,并对其进行负调控,CSE是肝脏中H2S产生的主要来源。机制上,MPST通过抑制CSE /

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    2024-04-23 ms3000001175451525 来自河北省

    学习了。

    0

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    2017-10-17 lyh994

    分子水平的研究

    0

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    2017-10-16 一米阳光的温暖

    学习了

    0

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    2017-10-16 Y—xianghai

    学习了新知识

    0

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    2017-10-16 tanxingdoctor

    学习啦!谢谢分享

    0

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