背景:肥胖是一种常见的公共卫生问题,目前被认为是一种疾病。研究表明,肥胖个体患胆结石的风险升高。本研究旨在探讨肥胖与正常体重胆石症患者胆汁蛋白质组学差异。
方法:在我们中心接受腹腔镜胆囊切除术的20名患者(10名肥胖患者和10名正常体重患者)的胆汁样本进行串联质量标签标记(TMT)和液相色谱-串联质谱(LC-MS/MS),其次是进一步的生物信息学分析。
结果:在差异表达的蛋白质中,23个上调,67个下调。生物信息学分析表明,这些差异表达蛋白主要参与细胞发育,炎症反应,甘油脂代谢过程,和蛋白质激活级联。此外,过氧化物酶体增殖物激活受体的活性(PPAR,在京都基因和基因组百科全书(KEGG)富集分析中,核受体亚家族)信号通路降低。PPAR信号通路中的两个下调蛋白,APOA-I和APOA-II,使用酶联免疫吸附试验证实。
结论:PPAR信号通路可能在肥胖患者胆石症的发生发展中起关键作用。此外,胆结石患者的胆道蛋白质组学分析揭示了肥胖,为今后的研究提供参考。
BACKGROUND: Obesity is a common public health issue and is currently deemed a disease. Research has shown that the risk of gallstones in individuals with obesity is elevated. This study aimed to explore the bile proteomics differences between cholelithiasis patients with obesity and normal body weight.
METHODS: Bile samples from 20 patients (10 with obesity and 10 with normal body weight) who underwent laparoscopic cholecystectomy at our center were subjected to tandem mass tag labeling (TMT) and liquid chromatography-tandem mass spectrometry (LC-MS/MS), followed by further bioinformatic analysis.
RESULTS: Among the differentially expressed proteins, 23 were upregulated and 67 were downregulated. Bioinformatic analysis indicated that these differentially expressed proteins were mainly involved in cell development, inflammatory responses, glycerolipid metabolic processes, and protein activation cascades. In addition, the activity of the peroxisome proliferator-activated receptor (PPAR, a subfamily of nuclear receptors) signaling pathway was decreased in the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Two downregulated proteins in the PPAR signaling pathway, APO A-I and APO A-II, were confirmed using enzyme-linked immunosorbent assay.
CONCLUSIONS: The PPAR signaling pathway may play a crucial role in the development of cholelithiasis among patients with obesity. Furthermore, biliary proteomics profiling of gallstones patients with obesity is revealed, providing a reference for future research.