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Thromb Haemost:增加人类凝血因子活性和表达的不是脂肪肝!

2017-05-25 吴刚 环球医学

2017年1月,发表在《Thromb Haemost》的一项研究,得出了会增加人类凝血因子活性和表达的是肥胖或胰岛素抵抗而非肝脏脂肪的结论。肝脏脂肪的增加可因胰岛素抵抗和脂肪组织炎症造成,或由rs738409中的PNPLA3的常见I148M变异体造成,但是脂肪肝缺乏这些特征。研究人员假设,是肥胖/胰岛素抵抗而非肝脏脂肪增加循环凝血因子活性。我们测量了92名研究对象的凝血酶原时间(PT)、活化部分凝

2017年1月,发表在《Thromb Haemost》的一项研究,得出了会增加人类凝血因子活性和表达的是肥胖或胰岛素抵抗而非肝脏脂肪的结论。

肝脏脂肪的增加可因胰岛素抵抗和脂肪组织炎症造成,或由rs738409中的PNPLA3的常见I148M变异体造成,但是脂肪肝缺乏这些特征。研究人员假设,是肥胖/胰岛素抵抗而非肝脏脂肪增加循环凝血因子活性。我们测量了92名研究对象的凝血酶原时间(PT)、活化部分凝血酶时间(APTT)、一些凝血因子的活性、VWF:RCo和纤维蛋白原、D-二聚体的血浆浓度。这些研究对象的分组基于胰岛素灵敏性(胰岛素抵抗(IR)vs胰岛素敏感(IS))和PNPLA3基因(PNPLA3148MM/MI vs PNPLA3148II)。与IS(6±1%,P<0.05)和PNPLA3148II(8±1%,P<0.05)相比,IR(13±1%)和PNPLA3148MM/MI(12±2%)患者的肝脏脂肪含(1H-MRS)的增加相似。与IS相比,IR的FVIII、FIX、FXIII、纤维蛋白原和VWF:RCo的活性都增加,PT和APTT缩短,与PNPLA3148MM/MI和PNPLA3148II组间这些活性的相似相反。经行肝脏活检和完全缺乏I148M变异体的患者中,胰岛素抵抗患者比相同肥胖的胰岛素敏感患者具有较高的F8、F9和FGG肝脏表达。脂肪组织中促炎性基因的表达与PT(%正常值)、循环FVIII、FIX、FXI、VWR:RCo和纤维蛋白原正相关,抗炎症基因的表达与PT(%)、FIX和纤维蛋白原负相关。我们得出结论,肥胖/胰岛素抵抗而非肝脏脂肪的增加,与促凝血因子的血浆特征相关。这反映了脂肪组织炎症和凝血因子肝脏产生的增加及其活化的易感性。

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    2018-02-19 changfy
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    2017-06-15 laoli

    谢谢分享!学习了!

    0

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    2017-05-26 惠映实验室

    糖尿病患者较容易凝血?

    0

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    2017-05-25 1ddf0692m34(暂无匿称)

    学习了,涨知识

    0

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