MRPMedical Research and Practice2993-96902993-9704Art and Technology10.61369/MRP.2026090026Article消渴固肾方干预2型糖尿病模型大鼠血清代谢重塑的非靶向代谢组学研究https://artdesignp.com/journal/MRP/4/9/10.61369/MRP.2026090026赵争敏,齐红朝,李欣,吴佳丽,吴晓芹,郑靓2026492026-09-20目的：基于LC-MS 非靶向血清代谢组学，解析消渴固肾方对高脂饮食联合链脲佐菌素诱导2型糖尿病大鼠血清代谢重塑的作用。方法：设正常、模型、消渴固肾方低/ 中/ 高剂量、阳性对照及QC 组，行LC-MS 采集、差异分析、PCA/PLS-DA、KEGG 富集及WGCNA 分析。结果：纳入34个样本，获690个代谢特征，映射率88.41%。模型组较正常组筛得109个差异代谢物（63个上调、46个下调），富集于胆汁分泌、鞘脂代谢及甾体激素生物合成通路。低、中、高剂量组分别筛得75、61、55个差异代谢物，PC(16:0/20:5) 在三组均呈反向调节。WGCNA 识别5个模块，筛选出SM(d18:0/16:1)、氢化可的松、胆酸等候选关键代谢物。结论：消渴固肾方系统性重塑T2DM 大鼠血清代谢组，涉及胆汁酸、鞘脂代谢及甾体激素合成通路，为后续机制验证提供候选靶点。消渴固肾方,2 型糖尿病,非靶向代谢组学,胆汁酸,鞘脂代谢,WGCNA

[1] Rinschen MM, et al. Metabolomics and lipidomics in metabolic disease research. Cell Metabolism, 2019.[2] Reed MJ, Meszaros K, Entes LJ, et al. A new rat model of type 2 diabetes: the fat-fed, streptozotocin-treated rat. Metabolism, 2000.[3] 赵争敏, 齐红朝, 杨宏杰, 等. 消渴固肾方对2 型糖尿病大鼠尿微量白蛋白的影响及机制研究[J]. 中文科技期刊数据库( 全文版) 医药卫生,2023(5):0092-0095.[4]Zhang A, Sun H, Wang P, et al. Metabonomics for discovering biomarkers of diabetes mellitus. Journal of Proteome Research, 2016.[5] 周迎生, 高妍, 李斌, 等. 高脂喂养联合链脲佐菌素注射的糖尿病大鼠模型特征[J]. 中国实验动物学报,2005,(3):154-158+196.[6] Dunn WB, Broadhurst D, Begley P, et al. Procedures for large-scale metabolic profiling of serum and plasma using gas chromatography and liquid chromatography coupledto mass spectrometry. Nature Protocols, 2011.[7] Langfelder P, Horvath S. WGCNA: an R package for weighted correlation network analysis. BMC Bioinformatics, 2008.[8] Wahlström A, Sayin SI, Marschall HU, Bäckhed F. Intestinal crosstalk between bile acids and microbiota and its impact on host metabolism. Cell Metabolism, 2016.[9] Chaurasia B, Summers SA. Ceramides—lipotoxic inducers of metabolic disorders. Trends in Endocrinology & Metabolism, 2015.[10] Sumner LW, et al. Proposed minimum reporting standards for chemical analysis (metabolomics standards initiative). Metabolomics, 2007.