Diabetologia:表观遗传修饰基因Zfp/ZNF423控制脂肪形成的作用?

2018-04-24 MedSci MedSci原创

近日,国际杂志 《Diabetologia》上在线发表一项关于表观遗传修饰基因Zfp/ZNF423控制小鼠脂肪形成的作用并在人肥大性肥胖症中异常表达的研究。 皮下脂肪细胞肥大与胰岛素抵抗和2型糖尿病风险增加有关,并可预测未来发展。在人类中,皮下脂肪组织肥大是脂肪前体细胞向脂肪形成途径受损,而不是前体细胞的缺乏的结果。被称为锌指蛋白(ZFP)423的锌指转录因子已被确定为前脂肪细胞形成的主要决

近日,国际杂志 《Diabetologia》上在线发表一项关于表观遗传修饰基因Zfp/ZNF423控制小鼠脂肪形成的作用并在人肥大性肥胖症中异常表达的研究。 皮下脂肪细胞肥大与胰岛素抵抗和2型糖尿病风险增加有关,并可预测未来发展。在人类中,皮下脂肪组织肥大是脂肪前体细胞向脂肪形成途径受损,而不是前体细胞的缺乏的结果。被称为锌指蛋白(ZFP)423的锌指转录因子已被确定为前脂肪细胞形成的主要决定因素并保持白色脂肪细胞功能。尽管在脂肪形成过程中其水平不变,但非脂肪源性鼠细胞中Zfp423的异位表达足以激活编码过氧化物酶体增殖物激活受体γ(Pparγ;也称为Pparg)并增加这些细胞的脂肪形成潜力。研究人员调查了Zfp423基因是否处于表观遗传调控之下,以及它是否在与肥大性肥胖相关的限制性脂肪形成中发挥作用。 鼠3T3-L1和NIH-3T3细胞分别用作定向和未定向脂肪细胞谱系的成纤维细胞。人类前脂肪细胞从具有宽脂肪细胞大小范围的20个瘦型非糖尿病个体的皮下脂肪组织的基质血管部分分离。通过实时定量PCR测量mRNA水平,而通过亚硫酸氢盐测序分析甲基化水平。通过微球菌核酸酶保护测定分析染色质结构

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