文献类型：期刊文献

英文题名：Microbiota-Targeted Chitooligosaccharides Intervention Restores Glucose Homeostasis After Islet Cell Transplantation in Rapamycin-Treated Mice

作者：Chang, Kunlin[1];He, Duowen[2];Dong, Junfeng[2];Zhang, Yayu[1];Deng, Shuxin[1];Zhao, Mengyao[1,3];Jin, Jiayang[1];Ji, Xiaoguo[1,4];Yin, Hao[2,4];Zhao, Liming[1,4,5]

机构：[1]East China Univ Sci & Technol, Sch Biotechnol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]Naval Med Univ, Shanghai Changzheng Hosp, Affiliated Hosp 2, Organ Transplant Ctr, Shanghai, Peoples R China;[3]Shanghai Frontiers Sci Ctr Optogenet Tech Cell Met, Shanghai, Peoples R China;[4]Shanghai Collaborat Innovat Ctr Biomfg Technol SCI, Shanghai, Peoples R China;[5]East China Univ Sci & Technol, Med Engn Integrat Innovat Ctr, Shanghai, Peoples R China

年份：2026

卷号：14

期号：7

外文期刊名：FOOD SCIENCE & NUTRITION

收录：;Scopus(收录号：2-s2.0-105044901546);WOS:【SCI-EXPANDED(收录号:WOS:001822370200001)】；

基金：This work was supported by the Shanghai Sailing Program (23YF1409800), the Young Scientists Fund of the National Natural Science Foundation of China (32302102), and the Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism (Shanghai Municipal Education Commission) and Shanghai Collaborative Innovation Center for Biomanufacturing Technology.

语种：英文

外文关键词：chitooligosaccharides; glucose homeostasis; gut microbiota; islet cell transplantation; rapamycin

摘要：Islet cell transplantation (ICT) is an effective treatment for diabetes mellitus, but postoperative islet function recovery and inflammation are closely linked to immunosuppressants. Using multi-omics and fecal microbiota transplantation (FMT) in human microbiota-associated (HMA) mice, this study explored rapamycin-induced gut dysbiosis and its impacts on islet function and inflammation post-ICT. ICT significantly altered the gut microbiota of type 2 diabetes mellitus (T2DM) patients, and FMT from these patients to antibiotic-treated mice recapitulated metabolic disorders in the mice. These disorders included hyperglycemia, hepatic and pancreatic injury, and impaired intestinal barrier. Rapamycin decreased beneficial bacteria (Akkermansia, Faecalibacterium) and enriched Desulfovibrio in HMA-T2DM mice. Targeted microbial modulation by chitooligosaccharides (COS) ameliorated rapamycin-induced deficits in insulin and C-peptide secretion, as well as elevated glycated hemoglobin levels. COS also significantly reduced serum inflammatory markers IP-10 and MCP-1, while upregulating colonic barrier proteins (Muc2, Occludin) in HMA-T2DM-ICT mice. COS additionally mitigated postoperative hyperglycemia via the PI3K/AKT/GSK3 beta/FOXO1 signaling pathway. This study identified COS as a microbiota-targeted adjunctive strategy to improve metabolic recovery and islet function under post-transplant immunosuppression.