糖尿病与胰腺癌存在复杂的双向关系，糖尿病患者患胰腺癌的风险升高，胰腺癌也会加重糖尿病的病情。近年研究发现，经典降糖药物二甲双胍不仅能改善糖代谢，还在胰腺癌的治疗和预防中有潜在的抗肿瘤作用。其抗癌机制激活腺苷酸活化蛋白激酶（AMPK）、抑制哺乳动物雷帕霉素靶蛋白（mTOR）信号通路、调控糖代谢重编程、降低炎症和氧化应激，发挥抗癌作用。二甲双胍还能下调程序性死亡配体-1（PD-L1）表达改善免疫微环境，增强化疗敏感性，抑制肿瘤生长及转移。临床研究进一步支持二甲双胍能够降低糖尿病患者胰腺癌的发病率，改善胰腺癌术后患者预后，并与其他化疗药物存在协同效应。但二甲双胍的抗癌作用机制及最佳治疗方案仍需进一步研究。

There is a complex bidirectional relationship between diabetes and pancreatic cancer, with diabetic patients having a significantly higher risk of developing pancreatic cancer and the development of pancreatic cancer exacerbating diabetes. Metformin, a classic hypoglycemic drug, has been shown in recent years not only to improve glucose metabolism, but also to have potential antitumor effects in the treatment and prevention of pancreatic cancer. Studies have shown that metformin exerts anticancer effects by activating adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK), inhibiting the mammalian target of rapamycin (mTOR) signaling pathway, modulating the reprogramming of glucose metabolism, and reducing inflammation and oxidative stress. In addition, metformin improves the immune microenvironment by downregulating programmed cell death ligand 1 (PD-L1) expression, increases chemotherapy sensitivity, and inhibits tumor growth and metastasis. Clinical studies also support the ability of metformin to reduce the incidence of pancreatic cancer in diabetic patients, improve the prognosis of postoperative pancreatic cancer patients, and show synergistic effects with other chemotherapeutic agents. However, the mechanism of anticancer effects of metformin and the optimal therapeutic regimens still need to be further investigated.

R285.5

云南省兴滇英才计划青年人才专项；云南省教育厅科学研究基金项目（2023J0543）