【摘要】 Barrett食管（BE）是食管下段鳞状上皮向柱状上皮化生的病理状态，通常与胃食管反流病（GERD）密切相关，是食管腺癌（EAC）的主要癌前病变。肥胖已成为全球性健康问题，被认为是GERD和BE的重要危险因素，其不仅通过机械性压力增加胃食管反流，还可能通过代谢异常和慢性低度炎症等机制直接促进BE的发生和进展为EAC。肥胖所致腹腔压力升高、下食管括约肌功能障碍及食管蠕动异常均可加剧GERD，诱发BE；同时，肥胖相关的代谢紊乱，如胰岛素抵抗与高胰岛素血症，可通过促进细胞增殖、诱发炎症反应及加重反流，增加BE风险；脂肪因子在BE发生中的作用亦不容忽视，瘦素通过促炎和促进细胞增殖参与BE形成，脂联素则可能通过抗炎和抑制异常增殖对BE具有保护作用；此外，肥胖诱导的慢性低度炎症在BE发生中发挥关键作用。通过探讨肥胖与BE发生与发展为EAC的关联及其潜在机制，可为深入理解BE的病理基础及制定防控策略提供参考。更多还原

【Abstract】 Barrett’s esophagus(BE) is a pathological condition characterized by the metaplasia of squamous epithelium to columnar epithelium in the lower esophagus, commonly associated with gastroesophageal reflux disease(GERD) and serving as the primary precancerous lesion for esophageal adenocarcinoma(EAC). Obesity has become a global health concern and is recognized as a significant risk factor for GERD and BE. It not only increases gastroesophageal reflux through mechanical pressure but may also directly promote the development and progression of BE via metabolic abnormalities and chronic low-grade inflammation. Elevated intra-abdominal pressure, lower esophageal sphincter dysfunction, and impaired esophageal motility caused by obesity can exacerbate GERD, thereby inducing BE. Additionally, obesity-related metabolic disorders, such as insulin resistance and hyperinsulinemia, may increase BE risk by promoting cell proliferation, triggering inflammatory responses, and worsening reflux. The role of adipokines in BE pathogenesis is also noteworthy; leptin contributes to BE formation through pro-inflammatory and pro-proliferative effects, while adiponectin may exert a protective role via anti-inflammatory and anti-proliferative mechanisms. Furthermore, obesity-induced chronic low-grade inflammation plays a crucial role in BE development. By summarizing the association between obesity and the initiation and progression of BE to EAC, along with its underlying mechanisms, this study provides references for understanding the pathological basis of BE and formulating potential prevention strategies.更多还原