Li Xuan, Watanabe Keita, Kimura Ikuo
Department of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Japan.
AMED-CREST, Japan Agency for Medical Research and Development, Tokyo, Japan.
Front Immunol. 2017 Dec 20;8:1882. doi: 10.3389/fimmu.2017.01882. eCollection 2017.
Accumulating evidence over the past decade has linked the development of metabolic syndrome related to diabetes to variations in gut microbiota, an emerging, critical homeostatic regulator of host energy metabolism and immune responses. Mechanistic studies in rodent models have revealed an ever-increasing multitude of molecular mechanisms whereby the gut microbiota interacts with various host sensing and signaling pathways, leading to modulation of endocrine system, immune responses, nervous system activity, and hence, the predisposition to metabolic diseases. Remarkably, the microbiota-driven immune responses in metabolic tissues and the host nutrient-sensing mechanisms of gut microbial metabolites, in particular short-chain fatty acids, have been significantly associated with the proneness to diabetes and related disorders. This review will synthesize the recent efforts on unraveling the mediating role of gut microbiota in the pathogenesis of metabolic diseases, aiming to reveal new therapeutic opportunities.
在过去十年中,越来越多的证据表明,与糖尿病相关的代谢综合征的发展与肠道微生物群的变化有关,肠道微生物群是宿主能量代谢和免疫反应中一个新出现的关键稳态调节因子。对啮齿动物模型的机制研究揭示了越来越多的分子机制,通过这些机制,肠道微生物群与各种宿主传感和信号通路相互作用,导致内分泌系统、免疫反应、神经系统活动的调节,进而导致代谢疾病的易感性。值得注意的是,微生物群驱动的代谢组织中的免疫反应以及肠道微生物代谢产物(特别是短链脂肪酸)的宿主营养传感机制,与糖尿病及相关疾病的易感性显著相关。本综述将综合最近在揭示肠道微生物群在代谢疾病发病机制中的介导作用方面所做的努力,旨在揭示新的治疗机会。