Zhang Lijing, Zhou Wen, Zhan Libin, Hou Shenglin, Zhao Chunyan, Bi Tingting, Lu Xiaoguang
School of Traditional Chinese Medicine and School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Department of Emergency Medicine, Zhongshan Hospital, Dalian University, Dalian 116001, China.
Aging (Albany NY). 2020 Sep 12;12(17):17480-17502. doi: 10.18632/aging.103756.
Obesity is one of the susceptibility factors for type 2 diabetes (T2DM), both of which could accelerate the aging of the body and bring many hazards. A causal relationship is present between intestinal microbiota and body metabolism, but how the microbiota play a role in the progression of obesity to T2DM has not been elucidated. In this study, we transplanted healthy or obese-T2DM intestinal microbiota to ZDF and LZ rats, and used 16S rRNA and targeted metabonomics to evaluate the directional effect of the microbiota on the susceptibility of obese rats to T2DM. The glycolipid metabolism phenotype could be changed bidirectionally in obese rats instead of in lean ones. One possible mechanism is that the microbiota and metabolites alter the structure of the intestinal tract, and improve insulin and leptin resistance through JAK2 / IRS / Akt pathway. It is worth noting that 7 genera, such as , and can regulate 15 metabolites, such as 3-indolpropionic acid, acetic acid and docosahexaenoic acid, and have a significant improvement on glycolipid metabolism phenotype. Attention to intestinal homeostasis may be the key to controlling obesity and preventing T2DM.
肥胖是2型糖尿病(T2DM)的易感因素之一,二者均可加速身体衰老并带来诸多危害。肠道微生物群与身体代谢之间存在因果关系,但微生物群在肥胖向T2DM进展过程中如何发挥作用尚未阐明。在本研究中,我们将健康或肥胖-T2DM肠道微生物群移植到ZDF和LZ大鼠体内,并使用16S rRNA和靶向代谢组学来评估微生物群对肥胖大鼠患T2DM易感性的定向影响。糖脂代谢表型在肥胖大鼠中可双向改变,而在瘦大鼠中则不然。一种可能的机制是微生物群和代谢产物改变肠道结构,并通过JAK2 / IRS / Akt途径改善胰岛素和瘦素抵抗。值得注意的是,诸如 、 和 等7个属可调节如3-吲哚丙酸、乙酸和二十二碳六烯酸等15种代谢产物,并对糖脂代谢表型有显著改善。关注肠道稳态可能是控制肥胖和预防T2DM的关键。