Nat Genet:三重磅:那些怎么都瘦不了的胖子们,你们可能是体内这个重要基因坏了

2018-01-10 王新凯 奇点网

前几天,基因检测公司23andMe宣布,他们要在2018年开展一项划时代的研究。而且这项邀请了全球130万人参与(最终符合条件的参与人数超过10万)的大型研究,只为解答一个减肥界的未解之谜

前几天,基因检测公司23andMe宣布,他们要在2018年开展一项划时代的研究。而且这项邀请了全球130万人参与(最终符合条件的参与人数超过10万)的大型研究,只为解答一个减肥界的未解之谜:

吃的都是一个锅里的饭,为啥一个瘦一个胖?报的都是同一个减肥班,为啥有的人成功减肥20斤,而你竟然还胖了一丢丢?

消息一出,质疑之声也随之而来。一个做基因检测的公司如此兴师动众,誓要证明减肥效果和你的基因有关,难免会让人猜测,是不是又忽悠我去做基因检测啊?

这其中的商业考量暂且不论,我们今天要说的是,就在2018年1月8日,权威核心期刊《自然遗传学》(Nature Genetics)同时发表的三篇重磅文章明确指出,研究人员已经发现ADCY3基因突变可导致严重肥胖,并增加2型糖尿病的风险。

关于肥胖的话题,几乎已经是老生常谈了。据统计,全球目前共有19亿人被列为超重,其中6亿肥胖患者,不仅如此,全球学龄前小胖子的数量也已经高达4200万。全球肥胖人群史无前例地上升,对人类社会医疗保健造成了重大负担,不仅如此,肥胖还会导致包括2型糖尿病、心血管疾病、骨关节炎和癌症等疾病。

拯救胖子,早就不再是一句玩笑话,而是已经成为全球科学家们面对的一个严肃课题。

正如文章开头所提到的那个减肥界的未解之谜,肥胖并不总是暴饮暴食或不运动的问题,那么无疑肥胖症是一种受到遗传因素和环境因素共同影响的疾病。

而且在大家的感受中,肥胖也好像就是一种最容易遗传的疾病之一,甚至我们还能说出许多目睹大街上大胖子牵着小胖子逛街的经历。但目前为止,科学家们并没有找到大部分肥胖病例的遗传病因。

在之前的研究中,科学家已经证明,瘦素-黑皮质素信号途径在控制能量稳态、食欲和体重方面发挥着关键作用。然而,涉及这条信号通路的一些基因功能丧失性突变,只能解释不到5%的肥胖病例。

2015年,英国帝国理工学院的研究人员在巴基斯坦近亲族群中发现,一些肥胖相关基因突变(LEP、LEPR和MC4R)可解释约30%的严重肥胖病例。隐性突变其实是一个高中生物学知识。可以简单地理解为本来好好的基因型AA,哪天不知道怎么地就突变成了Aa。当然,作为一个隐形突变,如果想要表现出突变性状(可以理解为发病),起码得等到两个都是Aa基因型的人结婚,这样其后代才有四分之一的概率是aa基因型。

其实很多类似的隐形遗传基因病,其患病概率还是蛮低的。但是,如果在一个血缘关系亲近的封闭族群中,就不一样了,隐性突变发病的概率将会大大升高(这也就是自古以来不能近亲通婚的原因)。

这事儿我们完全可以倒过来思考。其实,在当今人类社会中,想要找到一些相对比较封闭和遗传稳定的人类族群并不容易,而且都是遗传学家们的重点喜爱对象。

英国帝国理工学院的研究人员也是如此。他们认为在巴基斯坦的这个族群中,或许可以鉴定出与肥胖有关的新的单基因遗传突变。

于是,帝国理工学院的Philippe Froguel和他的同事,对巴基斯坦旁遮普省一个近亲家族中的138名严重早发性肥胖症患者及117名家庭成员,进行了全外显子组测序(WES)。果然,研究人员鉴定出4名来自三个不相关家族的严重肥胖儿童,具有之前从未发现的ADCY3纯合突变(包括一个移码突变、一个剪接位点突变和非同义错义突变)。值得注意的是,研究人员在筛选和鉴定的过程,没有报告任何其他可能导致单基因肥胖的隐性突变。


在四个受影响的家庭中鉴定ADCY3突变过程

此外,研究人员还对一个非同族的欧洲-美国血统肥胖家庭儿童进行了外显子测序,发现一个影响ADCY3的复合杂合突变。研究人员指出,ADYC3中所有这些突变位点都是高度保守的,这表明它们具有进化意义,而且这些突变都可能会影响ADYC3蛋白的功能。

和Philippe Froguel团队对巴基斯坦族群的研究一样,格林兰岛上的因纽特人,也成了丹麦哥本哈根大学研究人员的重点喜爱对象。研究人员在格陵兰人群中同样发现了ADCY3遗传变异,这些突变导致ADCY3相关RNA表达的降低,而且其与肥胖症和2型糖尿病风险显着增加有关。

说到这一步,我们不禁要问,一个基因突变真的可以导致严重肥胖吗?

其实在此之前,科学家们已经在小鼠实验中发现,敲除ADYC3的小鼠会食欲增加并变得肥胖,而且如果只选择性消融该基因在下丘脑中表达,也会导致小鼠身体脂肪量的增加。此外还有研究表明,那些ADYC3功能获得性突变的小鼠具有比野生型小鼠更少的身体脂肪,并且在高脂饮食喂养中对肥胖有着显着的抵抗。

帝国理工和哥本哈根大学的这两项人类遗传学研究,就正是ADCY3遗传突变会导致严重肥胖人类患者的结果和证据。

ADCY3遗传突变又是如何导致肥胖的呢?在同日发表的第三篇重磅研究中,加州大学旧金山分校的研究人员揭示,ADCY3(腺苷酸环化酶3)蛋白和MC4R(黑色素皮质素受体)共同定位于下丘脑某些神经元的初级纤毛(primary cilia),这些神经元影响着大脑的能量稳态和摄食行为,而这些初级纤毛影响着神经元之间的信号传导,ADCY3蛋白和MC4R蛋白则又是相关信号转导的重要物质。


小鼠下丘脑神经元(红色,蓝色为细胞核)和它们的初级纤毛(绿色)

如果出现了影响这两种蛋白质功能的基因突变,则会影响下丘脑有关能量稳态和摄食行为的信号传导,从而导致严重的肥胖,并且增加2型糖尿病的风险。

ADCY3、MC4R以及未来更多基因突变对肥胖影响的揭示,或许真的能给出了一个答案,你之所以胖,或者你怎么都减不下来,可能就是某个基因的问题。Philippe Froguel教授对此就表示,“正如通常大家所说的那样,肥胖并不总是暴饮暴食的问题,我认为,考虑到新的治疗方法正在变得可能,我们应该有一个积极的前景。”

研究肥胖症及相关疾病的遗传因素,对于寻找相关治疗方法是非常有价值的。虽然目前有一些药物可用或正在接受测试,但是如果清楚什么样的突变会导致肥胖,科学家们就可以制造出针对性的更有效的药物。

原始出处:

[1]Sadia Saeed, Amélie Bonnefond, et al. Loss-of-function mutations in ADCY3 cause monogenic severe obesity. Nature Genetics (2018)


[3]Niels Grarup, Ida Moltke, Mette K. Andersen, et al. Loss-of-function variants in ADCY3 increase risk of obesity and type 2 diabetes. Nature Genetics (2018)

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    2018-02-21 cy0324
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    2018-05-21 liye789132251
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    2018-02-05 Tulipzyz

    基因.好高深啊

    0

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    2018-01-12 xxxx1054
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    2018-01-11 虈亣靌

    学习一下谢谢分享

    0

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    2018-01-11 飛歌

    学习了很有用

    0

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