Fontaine Eric
INSERM, LBFA Université Grenoble Alpes, Grenoble, France.
Front Endocrinol (Lausanne). 2018 Dec 17;9:753. doi: 10.3389/fendo.2018.00753. eCollection 2018.
Metformin is the most widely prescribed drug to treat patients with type II diabetes, for whom retrospective studies suggest that metformin may have anticancer properties. However, in experiments performed with isolated cells, authors have reported both pro- and anti-apoptotic effects of metformin. The exact molecular mechanism of action of metformin remains partly unknown despite its use for over 60 years and more than 17,000 articles in PubMed. Among the various widely recognized or recently proposed targets, it has been reported consistently that metformin is capable of inhibiting mitochondrial respiratory chain Complex I. Since most of the effects of metformin have been replicated by other inhibitors of Complex I, it has been suggested that the mechanism of action of metformin involved the inhibition of Complex I. However, compared to conventional Complex I inhibitors, the metformin-induced inhibition of Complex I has unique characteristics. Among these, the most original one is that the concentrations of metformin required to inhibit Complex I are lower in intact cells than in isolated mitochondria. Experiments with isolated mitochondria or Complex I were generally performed using millimolar concentrations of metformin, while plasma levels remain in the micromolar range in both human and animal studies, highlighting that metformin concentration is an important issue. In order to explain the effects in animals based on observations in cells and mitochondria, some authors proposed a direct effect of the drug on Complex I involving an accumulation of metformin inside the mitochondria while others proposed an indirect effect (the drug no longer having to diffuse into the mitochondria). This brief review attempts to: gather arguments for and against each hypothesis concerning the mechanism by which metformin inhibits Complex I and to highlight remaining questions about the toxicity mechanism of metformin for certain cancer cells.
二甲双胍是治疗II型糖尿病患者最常用的药物,回顾性研究表明,二甲双胍可能具有抗癌特性。然而,在对分离细胞进行的实验中,作者报告了二甲双胍的促凋亡和抗凋亡作用。尽管二甲双胍已使用60多年,且PubMed上有超过17000篇相关文章,但其二甲双胍确切的分子作用机制仍部分未知。在各种广泛认可或最近提出的靶点中,一直有报道称二甲双胍能够抑制线粒体呼吸链复合体I。由于二甲双胍的大多数作用已被其他复合体I抑制剂所复制,因此有人提出二甲双胍的作用机制涉及对复合体I的抑制。然而,与传统的复合体I抑制剂相比,二甲双胍对复合体I的抑制具有独特的特征。其中,最独特的一点是,在完整细胞中抑制复合体I所需的二甲双胍浓度低于分离的线粒体。使用毫摩尔浓度的二甲双胍通常对分离的线粒体或复合体I进行实验,而在人类和动物研究中,血浆水平仍处于微摩尔范围内,这突出表明二甲双胍浓度是一个重要问题。为了解释基于细胞和线粒体观察结果在动物身上的效应,一些作者提出该药物对复合体I有直接作用,涉及二甲双胍在线粒体内的积累,而另一些作者则提出了间接作用(该药物不再需要扩散到线粒体内)。这篇简短的综述试图:收集支持和反对关于二甲双胍抑制复合体I机制的每种假设的论据,并突出关于二甲双胍对某些癌细胞毒性机制的剩余问题。