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肠道菌群改变与糖尿病发生相关
作者:小柯机器人 发布时间:2020/7/13 22:37:36

瑞典哥德堡大学Fredrik Bckhed研究团队揭示出肠道菌群在糖尿病前期以及糖尿病患者体内的改变。该项研究成果于2020年7月10日在线发表在《细胞—代谢》杂志上。

研究人员在一个发现(n=1011)和验证(n=484)队列中对肠道菌群进行了分析,该队列由未接受糖尿病治疗的瑞典受试者组成,并按血糖状况分组。研究人员观察到,糖耐量减低、葡萄糖不耐症以及2型糖尿病(T2D)的人群中肠道菌群的整体组成发生了改变,而空腹血糖受损的人则没有改变。
 
此外,在糖尿病前期和T2D组中,一些丁酸盐生产菌的丰度和丁酸盐生产的功能潜力均下降。多元分析和机器学习微生物组模型表明,胰岛素抵抗与微生物变异密切相关。因此,这项研究表明,在开发预防和/或延缓T2D的精确医学方法时,肠道菌群是一个重要的可变因素。
 
据介绍,肠道微生物群与T2D之间的联系值得进一步研究,因为已经知道抗糖尿病治疗会产生混杂效应。
 
附:英文原文

Title: The Gut Microbiota in Prediabetes and Diabetes: A Population-Based Cross-Sectional Study

Author: Hao Wu, Valentina Tremaroli, Caroline Schmidt, Annika Lundqvist, Lisa M. Olsson, Manuela Krmer, Anders Gummesson, Rosie Perkins, Gran Bergstrm, Fredrik Bckhed

Issue&Volume: 2020-07-10

Abstract: The link between the gut microbiota and type 2 diabetes (T2D) warrants further investigationbecause of known confounding effects from antidiabetic treatment. Here, we profiledthe gut microbiota in a discovery (n = 1,011) and validation (n = 484) cohort comprisingSwedish subjects naive for diabetes treatment and grouped by glycemic status. We observedthat overall gut microbiota composition was altered in groups with impaired glucosetolerance, combined glucose intolerance and T2D, but not in those with impaired fastingglucose. In addition, the abundance of several butyrate producers and functional potentialfor butyrate production were decreased both in prediabetes and T2D groups. Multivariateanalyses and machine learning microbiome models indicated that insulin resistancewas strongly associated with microbial variations. Therefore, our study indicatesthat the gut microbiota represents an important modifiable factor to consider whendeveloping precision medicine approaches for the prevention and/or delay of T2D.

DOI: 10.1016/j.cmet.2020.06.011

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30312-0

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx