【《Nature》——最新发现：肠道微生物抑制碳水化合物代谢，参与胰岛素抵抗】
研究表明，粪便碳水化合物（尤其是宿主可摄取的单糖）会在有胰岛素抵抗的个体中增加，并且与微生物的碳水化合物代谢和宿主炎症因子有关。

【题目】肠道微生物的碳水化合物代谢对胰岛素抵抗的影响

【摘要】胰岛素抵抗是代谢综合征和2型糖尿病的主要病理生理学基础。先前的宏基因组研究已经描述了肠道微生物群的特征及其在胰岛素抵抗中代谢主要营养物质的作用。尤其是有研究认为共生菌的碳水化合物代谢占宿主总能量摄取的10%，因此在肥胖和糖尿病的发病机制中发挥了重要作用。然而，其中的潜在机制仍不清楚。在本研究中，我们使用全面的多组学策略在人类中研究这种关系。我们将无偏向性的粪便代谢组学与宏基因组学、宿主代谢组学和转录组学的数据相结合，分析了微生物群参与胰岛素抵抗的情况。这些数据表明粪便碳水化合物（尤其是宿主可摄取的单糖）会在有胰岛素抵抗的个体中增加，并且与微生物的碳水化合物代谢和宿主炎症因子有关。我们发现了与胰岛素抵抗和胰岛素敏感相关的肠道细菌，这些细菌表现出特有的碳水化合物代谢模式，并且证明了与胰岛素敏感相关的细菌可以改善小鼠的胰岛素抵抗表型。我们的研究全面了解了胰岛素抵抗中宿主与微生物之间的关系，揭示了微生物群对碳水化合物代谢的影响，为改善胰岛素抵抗提供了潜在的治疗靶点。

英文原文

[Report] Faecal carbohydrates, particularly host-accessible monosaccharides, are increased in individuals with insulin resistance and are associated with microbial carbohydrate metabolisms and host inflammatory cytokines.

[Title] Gut microbial carbohydrate metabolism contributes to insulin resistance

[Authors] Tadashi Takeuchi, Tetsuya Kubota, Yumiko Nakanishi, Hiroshi Tsugawa, Wataru Suda, Andrew Tae-Jun Kwon, Junshi Yazaki, Kazutaka Ikeda, Shino Nemoto, Yoshiki Mochizuki, Toshimori Kitami, Katsuyuki Yugi, Yoshiko Mizuno, Nobutake Yamamichi, Tsutomu Yamazaki, Iseki Takamoto, Naoto Kubota, Takashi Kadowaki, Erik Arner, Piero Carninci, Osamu Ohara, Makoto Arita, Masahira Hattori, Shigeo Koyasu & Hiroshi Ohno

[Abstract] Insulin resistance is the primary pathophysiology underlying metabolic syndrome and type 2 diabetes1,2. Previous metagenomic studies have described the characteristics of gut microbiota and their roles in metabolizing major nutrients in insulin resistance3,4,5,6,7,8,9. In particular, carbohydrate metabolism of commensals has been proposed to contribute up to 10% of the host’s overall energy extraction10, thereby playing a role in the pathogenesis of obesity and prediabetes3,4,6. Nevertheless, the underlying mechanism remains unclear. Here we investigate this relationship using a comprehensive multi-omics strategy in humans. We combine unbiased faecal metabolomics with metagenomics, host metabolomics and transcriptomics data to profile the involvement of the microbiome in insulin resistance. These data reveal that faecal carbohydrates, particularly host-accessible monosaccharides, are increased in individuals with insulin resistance and are associated with microbial carbohydrate metabolisms and host inflammatory cytokines. We identify gut bacteria associated with insulin resistance and insulin sensitivity that show a distinct pattern of carbohydrate metabolism, and demonstrate that insulin-sensitivity-associated bacteria ameliorate host phenotypes of insulin resistance in a mouse model. Our study, which provides a comprehensive view of the host–microorganism relationships in insulin resistance, reveals the impact of carbohydrate metabolism by microbiota, suggesting a potential therapeutic target for ameliorating insulin resistance.

原文链接
http://t.cn/A6Ox6EXf