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《工程(英文)》 >> 2023年 第20卷 第1期 doi: 10.1016/j.eng.2022.09.010

硫化氢促进脂肪细胞分化、增生和肥大

a Cardiovascular and Metabolic Research Unit, Laurentian University, Sudbury, ON, P3E2C6, Canada
b Department of Biology, York University, Toronto, ON, M3J 1P3, Canada

收稿日期: 2021-12-12 修回日期: 2022-08-19 录用日期: 2022-09-25 发布日期: 2022-10-28

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摘要

硫化氢(H2S)在脂肪细胞和脂肪组织中内源性产生并刺激脂肪形成。然而,H2S 对肥胖症发展的综合致病作用及其潜在机制尚不清楚。本研究发现降低的内源性H2S水平降低了小鼠脂肪细胞中的脂质积累。在脂肪形成诱导6 d 后,外源性H2S 处理显著增加了原代小鼠前脂肪细胞的脂肪生成。在脂肪生成的早
期阶段,H2S增加细胞增殖并为细胞增生做好准备。H2S处理10 d 后,前脂肪细胞的细胞表面积和直径明显增大,表明细胞肥大。虽然H2S 刺激脂质积累和脂肪生成,但H2S 对脂肪分解没有影响。随着营养过载和高葡萄糖/胰岛素孵化,H2S 进一步刺激葡萄糖消耗并恶化脂肪细胞肥大。H2S 上调增生基因[CCAAT/增强子结合蛋白(C/EBPβ)、细胞分裂周期25(Cdc25)、微染色体维持3(Mcm3)和细胞分裂周期(Cdc45)]和细胞周期蛋白依赖性激酶2 蛋白(Cdk2),调节细胞增殖。H2S 还上调了胰岛素受体β(Irβ)激活的丝裂原活化蛋白激酶(MAPK)和蛋白激酶B(Akt)通路,从而导致脂肪生成。总之,H2S 增加脂肪细胞分化、肥大和增生,提示它在肥胖症中起致病作用。

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