JCEM:PCSK9的功能丧失变异能降低空腹和餐后脂肪及脂蛋白

2017-07-18 MedSci MedSci原创

低密度脂蛋白胆固醇(LDL-C)主要通过肝细胞表面的低密度脂蛋白受体(LDLR)清除。前蛋白转化酶枯草溶菌素9(PCSK9)是由肝脏合成的蛋白酶,释放入血后与LDLR结合,引导后者进入肝细胞后至溶酶体降解,从而减少肝细胞表面的LDLR数量,使血浆LDL-C水平升高。PCSK9基因的变异与PCSK9的功能丧失(LOF)相关,会导致肝LDLR的表达增加,LDL-C的浓度降低,以及预防心血管疾病(CVD

低密度脂蛋白胆固醇(LDL-C)主要通过肝细胞表面的低密度脂蛋白受体(LDLR)清除。前蛋白转化酶枯草溶菌素9(PCSK9)是由肝脏合成的蛋白酶,释放入血后与LDLR结合,引导后者进入肝细胞后至溶酶体降解,从而减少肝细胞表面的LDLR数量,使血浆LDL-C水平升高。

PCSK9基因的变异与PCSK9的功能丧失(LOF)相关,会导致肝LDLR的表达增加,LDL-C的浓度降低,以及预防血管疾病(CVD)。载脂蛋白B(apo)残粒也有助于预测心血管疾病的风险,且其清除途径同LDLR。研究人员假设功能丧失型PCSK9携带者的空腹和餐后残粒脂蛋白水平会显著降低。

来自加拿大的研究人员设计并进行了一项病例对照的代谢研究,在功能丧失型PCSK9携带者和无PCSK9变异对照组之间比较了空腹和餐后残余脂蛋白代谢指标——甘油三酯(TG)、总载脂蛋白B和apoB48含量。采用口服脂肪耐量试验作为干预。主要测量结果:在受试者口服脂肪后0、2、4、6小时测定受试者空腹和餐后血浆甘油三酯、apoB48,总apoB、总胆固醇和PCSK9。

研究发现,与无PCSK9变异的对照组(n = 23)相比,功能丧失型PCSK9携带者(n=22)的空腹LDL-C显著降低(-14%),空腹甘油三酯(-21%)也降低。PCSK9功能丧失的变异也能导致餐后总载脂蛋白B(-17%)、apoB48 (-23%)、和TG (-18%)的显著降低。功能丧失组和非变异组的餐后PCSK9水平都下降了(分别为-24%,-16%)。

功能丧失型PCSK9携带者的空腹和餐后TG、apoB48和总apoB水平降低。这可能能防止CVD的发生,未来需要进一步验证PCSK9抑制剂对降低CVD风险的作用。

原始出处:

Ooi TC, Krysa JA,et al.The Effect of PCSK9 Loss-of-Function Variants on the Postprandial Lipid and ApoB-Lipoprotein Response.J Clin Endocrinol Metab. 2017 Jun 30. doi: 10.1210/jc.2017-00684. [Epub ahead of print]

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    2017-10-29 smallant2015
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    2018-01-07 achengzhao
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    2018-02-17 FukaiBao
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    2017-08-02 Tamikia
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    2017-07-21 lou.minghong

    学习了谢谢分享!

    0

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    2017-07-19 天涯183

    非常好的文章,学习了,很受益

    0

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