Maya Magdy Abdelwahab, Ahmad S Ghattas, Ahmed Tawheed
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引用次数: 0
Abstract
The gut-liver-pancreas axis (GLPA) is a critical network shaped by gut microbiota (GM) and their metabolites, essential for maintaining metabolic and immune balance. Disruption of this microbial equilibrium, known as dysbiosis, contributes to the development and progression of various hepatic and pancreatic diseases. Through mechanisms such as increased intestinal permeability and exposure to microbial products-including lipopolysaccharide, trimethylamine-N-oxide, and secondary bile acids-dysbiosis promotes inflammation, oxidative stress, insulin resistance, and carcinogenesis. These changes are linked to conditions including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cirrhosis, hepatocellular carcinoma, pancreatitis, pancreatic ductal adenocarcinoma, and diabetes. Emerging tools like stool metagenomics and serum metabolomics help identify microbial biomarkers for diagnosis and risk stratification. While interventions such as probiotics, dietary changes, and fecal microbiota transplantation aim to restore microbial balance, their success remains inconsistent. This work aims to highlight the pathogenic role of GM across the GLPA, with special emphasis on the underexplored gut-pancreas connection. Advancing our understanding of the GLPA can unlock novel microbiota-targeted approaches for early diagnosis and treatment of hepatopancreatic diseases.
肠-肝-胰轴(GLPA)是由肠道微生物群(GM)及其代谢物形成的关键网络,对维持代谢和免疫平衡至关重要。这种微生物平衡的破坏,称为生态失调,有助于各种肝脏和胰腺疾病的发生和进展。通过增加肠道通透性和暴露于微生物产物(包括脂多糖、三甲胺- n -氧化物和继发性胆汁酸)等机制,生态失调会促进炎症、氧化应激、胰岛素抵抗和致癌。这些变化与代谢功能障碍相关的脂肪变性肝病、酒精相关肝病、肝硬化、肝细胞癌、胰腺炎、胰腺导管腺癌和糖尿病等疾病有关。新兴工具如粪便宏基因组学和血清代谢组学有助于识别诊断和风险分层的微生物生物标志物。虽然益生菌、饮食改变和粪便微生物群移植等干预措施旨在恢复微生物平衡,但其成功与否仍不一致。这项工作旨在强调转基因在GLPA中的致病作用,特别强调未被探索的肠道-胰腺连接。推进我们对GLPA的理解可以为肝胰腺疾病的早期诊断和治疗提供新的针对微生物群的方法。