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Nat Med:科学家发现「神药」二甲双胍降糖新机制,肠道微生物竟是重要一环!

2017-05-24 佚名 奇点网

二甲双胍作为降糖药,已经为II型糖尿病患者“服务”了几十年了,也是目前世界上应用最广泛的降糖药物。

1922年,两位科学家Emil Werner和James Bell发现了一个化合物——N,N-二甲基胍,它就是现在我们十分熟悉的二甲双胍。二甲双胍作为降糖药,已经为II型糖尿病患者“服务”了几十年了,也是目前世界上应用最广泛的降糖药物。



metformin-27699468_M近年来,二甲双胍被冠以“神药”之称,因为它不仅“老本行”干得好,还被陆续发现各种其他功效,比如降低胆固醇、抗衰老,甚至还能抗癌!然而回归“老本行”,这么多年来,研究人员们却一直没能完整地阐明它的作用机制。今天,新发表在《自然 医学》杂志上的研究证明,二甲双胍的降糖机制中,肠道微生物也发挥着重要作用!奇点糕忍不住要问,惊不惊喜?意不意外?

过去,研究人员一致认为,二甲双胍主要通过抑制肝脏中葡萄糖的产生来治疗糖尿病,而肝脏中一磷酸腺苷激活的蛋白激酶(adenosine monophosphate-activated protein kinase, AMPK)这一途径被发现也已经有十几年了。陆续的,又有研究人员发现AMPK不是唯一的作用途径,并且发现了新的机制。尽管已经有很多相关途径被发现,但是研究仍然没有停止。

近年来越来越多的研究结果提示我们,除了肝脏,肠道这一“器官”与二甲双胍发挥作用也有着不可分割的联系。例如,动物实验中发现口服二甲双胍比静脉注射的降糖效果更好;临床上的相关性研究也显示肠道微生物的改变对二甲双胍的降糖作用似乎有促进作用。Metformin-weight-loss

于是,为了探究出二甲双胍与肠道微生物之间究竟有怎样间接和直接的相互作用,来自瑞典和西班牙等国家的研究人员开展了一系列临床实验(EudraCT 2010-022394-34)。首先,为了知道二甲双胍会如何改变肠道微生物组成,研究人员对服用二甲双胍和服用安慰剂的两组志愿者进行了为期4个月的治疗,并且要求他们控制热量摄入,在治疗开始前以及开始后的2个月和4个月时收集了他们的粪便样本。



实验结束时,所有志愿者的身体质量指数(BMI)都下降了,但是粪便样本的测序显示,安慰剂组志愿者接受治疗后只有一种细菌的丰度发生了变化,而二甲双胍组在2个月和4个月时分别有81种和86种细菌发生了改变,其中Escherichia属细菌丰度增加明显,而Intestinibacter属下降明显。在第6个月时,安慰剂组部分改为服用二甲双胍,这部分志愿者的肠道微生物构成同样发生了改变。




不同属间微生物的相互作用,蓝色为服用二甲双胍前的积极相互作用,紫色为服用2个月后,灰色为消极相互作用

不但如此,他们还发现,二甲双胍能够增强不同属的微生物间的“积极相互作用”,尤其是变形菌门和厚壁菌门。

接下来,研究人员通过粪菌移植的方式,分别将三名二甲双胍组志愿者在治疗前后的肠道微生物“传递”给无菌小鼠,在移植后18天,对小鼠进行糖耐量测试。结果显示,接受了4个月二甲双胍组志愿者肠道微生物移植的小鼠在实验中表现更好,糖耐量提高,说明被二甲双胍改变的肠道微生物确实可以对糖耐量起到积极作用。

在验证了组成发生改变后,研究人员又着手对“功能改变”进行了研究。他们“翻出了”京都基因和基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG),这是研究代谢通路最主要的数据库,如果基因的功能发生了改变,那么自然它所对应的代谢通路也会发生改变。


三种短链脂肪酸的增加(横轴从左至右依次为乙酸、丙酸和丁酸),紫色为二甲双胍组,蓝色为安慰剂组,灰色为男性,白色为女性

对于服用了4个月安慰剂的志愿者来说,只有两条通路有变化,对比起来,二甲双胍组的数据简直是惊人的!服用了2个月的志愿者有626条通路上调,同时有130条下调;服用了4个月的相对减少了一些,分别有473条和69条。大量代谢通路的改变显然会影响到代谢产物的产量,通过定量分析,研究人员发现代谢产物中的一些有机短链脂肪酸,例如乙酸、丙酸和丁酸显着增加,这些短链脂肪酸对我们“宿主”是有益的。

除了短链脂肪酸,研究人员还意外的发现,二甲双胍组志愿者血液中胆汁酸的量也增加了。胆汁酸通常在脂肪代谢中起着重要作用,而在2014年,有研究人员发现,胆汁酸可以激活一种巨噬细胞上的受体,抑制II型糖尿病的炎症反应。尽管更早的时候就有研究发现,二甲双胍能够改变胆汁酸的分泌量,但是根本原因却没有被发现,这次,研究人员们“顺便”解决了这个“疑惑”。

biol481evol_piconumba2他们通过宏基因组测序,发现编码一种水解酶的基因bsh表达量增加,这种水解酶是由特定肠道微生物产生的,而它的作用就是水解胆汁中的胆盐,从而产生游离的胆汁酸。因此,当水解酶的量增加时,胆汁酸的量自然也就增加了。

最后,研究人员还建立了体外模型来探究二甲双胍对肠道微生物的直接影响,发现有两个门的细菌的蛋白编码基因受到二甲双胍的直接调节,样本中丰度最高的一个细菌A. muciniphila中有多达10%的蛋白编码基因都受到二甲双胍的调节(二甲双胍的“控制力”也是很惊人了)。



这个研究明确的向我们展示了,在二甲双胍复杂的降糖机制“列表”中,肠道微生物也要占据一席之位了,不知道未来II型糖尿病患者在服药前后是不是也可以为自己的肠道微生物测个序呢?

原始出处:

Hao Wu,Eduardo Esteve,Valentina Tremaroli, et al. Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. Nature Medicine (2017) doi:10.1038/nm.4345

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    2018-02-15 liye789132251
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    2017-05-25 惠映实验室

    肠道菌群是一个小型生态系统,既有共性,也有个性。

    0

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    2017-05-25 189****7206

    又是肠道微生物。

    0

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    2017-05-24 lovetcm

    二甲双胍,神

    0

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    2017-05-24 1e0f8808m18(暂无匿称)

    二甲双胍降糖新机制发现,巩固其基础降糖药地位。

    0

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