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二甲双胍通过调节糖尿病前期患者的肠道微生物群发挥抗肥胖作用:一种假说。

Metformin exerts anti-obesity effect via gut microbiome modulation in prediabetics: A hypothesis.

作者信息

Maniar Kunal, Moideen Amal, Bhattacharyya Rajasri, Banerjee Dibyajyoti

机构信息

Department of Pharmacology, Post Graduate Institute of Medical Education & Research, Chandigarh, India.

Department of Experimental Medicine & Biotechnology, Post Graduate Institute of Medical Education & Research, Chandigarh, India.

出版信息

Med Hypotheses. 2017 Jul;104:117-120. doi: 10.1016/j.mehy.2017.06.001. Epub 2017 Jun 1.

DOI:10.1016/j.mehy.2017.06.001
PMID:28673568
Abstract

Prediabetic individuals are characterized by high levels of insulin, an anabolic hormone having an important role in the maintenance of glucose homeostasis. However, insulin has also been found to increase the growth of certain bacteria which form the non-butyrate producing part of the gut microbiome. The gut microbiome is recently in focus for its strong association with many chronic diseases such as type 2 diabetes mellitus and obesity. Metformin, a widely popular anti-diabetic medication has been shown to prevent weight gain in many trials. There are many studies postulating the mechanisms of the anti-obesity effect of metformin including improvement in insulin sensitivity (and consequently a reduction in insulin levels). Recently, however, it is becoming evident that metformin's action is likely to be primarily mediated by the gut. Further, metformin has also shown to affect the growth characteristics of certain bacteria which form the part of the human gut microbiome. With this frame of reference in mind, we hypothesize that metformin is likely to exert its anti-obesity effect by altering the composition of the gut microbiome. If proved, this has the potential to contribute to the management of obesity and pave the way for the development of novel anti-obesity drugs.

摘要

糖尿病前期个体的特征是胰岛素水平较高,胰岛素是一种合成代谢激素,在维持葡萄糖稳态方面发挥着重要作用。然而,人们还发现胰岛素会促进某些细菌的生长,这些细菌构成了肠道微生物群中不产生丁酸盐的部分。最近,肠道微生物群因其与许多慢性疾病(如2型糖尿病和肥胖症)的密切关联而受到关注。二甲双胍是一种广受欢迎的抗糖尿病药物,在许多试验中已被证明可防止体重增加。有许多研究推测二甲双胍抗肥胖作用的机制,包括改善胰岛素敏感性(从而降低胰岛素水平)。然而,最近越来越明显的是,二甲双胍的作用可能主要由肠道介导。此外,二甲双胍还显示出会影响构成人类肠道微生物群一部分的某些细菌的生长特性。基于这一参考框架,我们假设二甲双胍可能通过改变肠道微生物群的组成来发挥其抗肥胖作用。如果得到证实,这有可能有助于肥胖症的管理,并为新型抗肥胖药物的开发铺平道路。

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