益生菌
肠道菌群
2型糖尿病
胰岛素抵抗
2型糖尿病
微生物群
代谢综合征
生物
转录组
脂肪组织
活性氧
脂质代谢
医学
下调和上调
糖尿病
抗氧化剂
微生物学
饮食性肥胖
抗性淀粉
化学
代谢途径
免疫学
大肠杆菌
双歧杆菌
β氧化
新陈代谢
内分泌学
胰岛素
肥胖
炎症
内科学
生物信息学
细菌
生物化学
药理学
作者
Congyang Mao,Wanyu Jin,Limeng Dou,Tong Guo,Jun Huang,Yi Wang,Xiangmei Liu,Shuilin Wu,Wei Qiao,Yiming Xiang,Yizhou Zhu,Jun Wu,K. W. Shadow Yeung
标识
DOI:10.1038/s41467-026-70138-3
摘要
The pandemic-scale progression of type 2 diabetes mellitus (T2DM) necessitates innovative interventions targeting the pathogenic triad of insulin resistance, dysregulation of lipid metabolism, and gut microbiome dysbiosis. Here, we report a synthetically bioengineered probiotic consortium (REcN-F/Ca) developed through directed metabolic adaptations of Escherichia coli Nissle 1917 (EcN) under iterative hydrogen peroxide selection, subsequently functionalized with fructooligosaccharide-calcium carbonate composites. REcN-F/Ca exhibits enhanced reactive oxygen species tolerance through upregulated antioxidant enzymes and hydrogen sulfide-mediated redox balancing, alongside improved gastrointestinal survivability. In high-fat diet-induced obese male mice, REcN-F/Ca restores gut microbiota diversity, enriches butyrogenic taxa (Lachnospiraceae and Blautia), and rescues short-chain fatty acids depletion. Transcriptomic profiling reveals PPAR signaling activation, driving lipid metabolism and suppressing adipose inflammation. These effects translate to systemic metabolic improvements with attenuated weight gain (−25.4%), restored glucose homeostasis, and reduced insulin resistance (HOMA-IR: −73.2%) in the obesity and T2DM murine model. Our findings establish REcN-F/Ca as a synthetically engineered probiotic that simultaneously corrects intestinal ecological perturbations and reverses host metabolic dysfunction, proposing a paradigm for metabolic syndrome management. Novel treatments are needed for type 2 diabetes mellitus which target insulin resistance, lipid metabolism dysregulation, and gut microbiome dysbiosis. Here the authors engineered a probiotic to tolerate oxidative stress, an alleviate type 2 diabetes in mice by activating host metabolic pathways.
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