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Nat Med:日本学者揭示肝荷尔蒙为何对运动减肥无效

摘要 : 2017年2月27日,国际学术权威刊物自然出版集团旗下子刊《Nature Medicine》杂志在线发表了日本金泽大学医学研究科Toshinari Takamura研究员的一篇研究论文,研究论文报道肝脏分泌的一种荷尔蒙作用于骨骼肌,会引起“运动抵抗性”的病态,导致运动效果差强人意。

 2017年2月27日,国际学术权威刊物自然出版集团旗下子刊《Nature Medicine》杂志在线发表了日本金泽大学大学院医学研究科Toshinari Takamura研究员的一篇研究论文,研究论文报道肝脏分泌的一种荷尔蒙作用于骨骼肌,会引起“运动抵抗性”的病态,导致运动效果差强人意。

一般常识认为,身体运动不足会引发肥胖、Ⅱ型糖尿病、高血压和脂肪肝等各种生活习惯病,因此定期运动对上述疾病进行预防和治疗是推荐做法。但是运动效果却千差万别,有些人即使做运动却仍不见效。

论文称,他们对Ⅱ型糖尿病、脂肪肝患者和高龄者多见的肝荷尔蒙“Hepatokine”(硒蛋白P浓度高)进行了研究。在小鼠和细胞实验中发现,过剩的硒蛋白P通过受容体“LRP1”(低密度脂蛋白受体相关蛋白)对肌肉起作用,引发使运动无效的“运动抵抗性”病态。而天生不具备硒蛋白P的小鼠与普通小鼠相比,在相同强度相同时间进行运动疗法,其运动效果倍增。研究小组继而在对健康者进行的临床研究中发现,经过8周有氧运动锻炼,血液中硒蛋白P浓度高的人比浓度低的人运动效果低很多。

研究明确了肝荷尔蒙是导致运动效果出现个人差的原因之一。医学报告显示,Ⅱ型糖尿病和脂肪肝患者、高龄者的血液中硒蛋白P浓度较高。

研究小组将以硒蛋白P和受容体LRP1为标靶,对其与Ⅱ型糖尿病等身体活动较少的各种生活习惯病的关联进行研究,以期开发出抑制肝脏生产硒蛋白P,以及增强运动效果的药物。

原文链接:

Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise in mice through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle

原文摘要:

Exercise has numerous health-promoting effects in humans1; however, individual responsiveness to exercise with regard to endurance or metabolic health differs markedly2, 3, 4. This 'exercise resistance' is considered to be congenital, with no evident acquired causative factors. Here we show that the anti-oxidative hepatokine selenoprotein P (SeP)5, 6, 7 causes exercise resistance through its muscle receptor low-density lipoprotein receptor–related protein 1 (LRP1)8. SeP-deficient mice showed a 'super-endurance' phenotype after exercise training, as well as enhanced reactive oxygen species (ROS) production, AMP-activated protein kinase (AMPK) phosphorylation9 and peroxisome proliferative activated receptor γ coactivator (Ppargc)-1α (also known as PGC-1α; encoded by Ppargc1a)10 expression in skeletal muscle. Supplementation with the anti-oxidant N-acetylcysteine (NAC) reduced ROS production and the endurance capacity in SeP-deficient mice. SeP treatment impaired hydrogen-peroxide-induced adaptations through LRP1 in cultured myotubes and suppressed exercise-induced AMPK phosphorylation and Ppargc1a gene expression in mouse skeletal muscle—effects which were blunted in mice with a muscle-specific LRP1 deficiency. Furthermore, we found that increased amounts of circulating SeP predicted the ineffectiveness of training on endurance capacity in humans. Our study suggests that inhibitors of the SeP–LRP1 axis may function as exercise-enhancing drugs to treat diseases associated with a sedentary lifestyle.

来源: Nature Medicine 浏览次数:0

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