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肠道微生物的碳水化合物代谢有助于胰岛素抵抗。

Gut microbial carbohydrate metabolism contributes to insulin resistance.

机构信息

Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Japan.

Intestinal Microbiota Project, Kanagawa Institute of Industrial Science and Technology, Kawasaki, Japan.

出版信息

Nature. 2023 Sep;621(7978):389-395. doi: 10.1038/s41586-023-06466-x. Epub 2023 Aug 30.

DOI:10.1038/s41586-023-06466-x
PMID:37648852
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10499599/
Abstract

Insulin resistance is the primary pathophysiology underlying metabolic syndrome and type 2 diabetes. Previous metagenomic studies have described the characteristics of gut microbiota and their roles in metabolizing major nutrients in insulin resistance. In particular, carbohydrate metabolism of commensals has been proposed to contribute up to 10% of the host's overall energy extraction, thereby playing a role in the pathogenesis of obesity and prediabetes. 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.

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组的特征及其在代谢胰岛素抵抗主要营养素中的作用。特别是，共生菌的碳水化合物代谢被认为可以贡献宿主总能量提取的 10%，从而在肥胖和糖尿病前期的发病机制中发挥作用。然而，其潜在机制尚不清楚。在这里，我们使用人类的综合多组学策略来研究这种关系。我们将无偏粪便代谢组学与宏基因组、宿主代谢组学和转录组学数据相结合，分析微生物组在胰岛素抵抗中的作用。这些数据表明，粪便中的碳水化合物，特别是宿主可利用的单糖，在胰岛素抵抗个体中增加，并与微生物碳水化合物代谢和宿主炎症细胞因子有关。我们鉴定了与胰岛素抵抗和胰岛素敏感性相关的肠道细菌，这些细菌表现出不同的碳水化合物代谢模式，并证明与胰岛素敏感性相关的细菌在小鼠模型中改善了宿主的胰岛素抵抗表型。我们的研究提供了胰岛素抵抗中宿主-微生物关系的全面视图，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一个潜在的治疗靶点。

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