肥胖是全球健康问题，与多种消化系统肿瘤密切相关。研究显示肥胖与食管腺癌、胃癌、结直肠癌、肝细胞癌、胆道癌、胰腺癌等消化系统肿瘤存在关联。本文阐述了肥胖通过代谢紊乱、慢性炎症、胰岛素抵抗、性激素异常等机制显著增加消化道肿瘤（如食管腺癌、胃癌、结直肠癌等）的发病风险，且风险随肥胖程度递增。脂肪细胞分泌的炎症因子可激活促炎信号通路，促进肿瘤细胞增殖；胰岛素抵抗导致高胰岛素血症，激活信号通路，酸化肿瘤微环境，利于肿瘤侵袭转移；性激素水平异常激活雌激素受体，促进肿瘤细胞生长。此外，肥胖诱导的肿瘤相关巨噬细胞（TAM）和癌症相关脂肪细胞（CAAs）通过分泌促炎因子和提供能量，进一步促进肿瘤发展。未来研究将聚焦肥胖与肿瘤的因果关系，开发针对相关靶点（如GPR65、PHD3、Glce）的药物，助力肥胖防控和肿瘤治疗。

Obesity is a global health issue closely related to various digestive system tumors. Studies have shown that obesity is associated with digestive system tumors such as esophageal adenocarcinoma, gastric cancer, colorectal cancer, hepatocellular carcinoma, biliary tract cancer, and pancreatic cancer. This article elaborates on how obesity significantly increases the risk of digestive tract tumors (such as esophageal adenocarcinoma, gastric cancer, and colorectal cancer) through mechanisms such as metabolic disorders, chronic inflammation, insulin resistance, and abnormal sex hormone levels. The risk increases with the degree of obesity. Inflammatory factors secreted by fat cells can activate pro-inflammatory signaling pathways and promote tumor cell proliferation; insulin resistance leads to hyperinsulinemia, activates signaling pathways, acidifies the tumor microenvironment, and facilitates tumor invasion and metastasis; abnormal sex hormone levels activate estrogen receptors and promote tumor cell growth. In addition, obesity-induced tumor-associated macrophages (TAMs) and cancer-associated adipocytes (CAAs) further promote tumor development by secreting pro-inflammatory factors and providing energy. Future research will focus on the causal relationship between obesity and tumors, and develop drugs targeting related targets (such as GPR65, PHD3, Glce) to assist in obesity prevention and control and tumor treatment.