Excessive fructose intake has been associated with the development and progression of pancreatic cancer. This study aimed to elucidate the relationship between fructose utilization and pancreatic cancer progression. Our findings revealed that pancreatic cancer cells have a high capacity to utilize fructose and are capable of converting glucose to fructose via the AKR1B1-mediated polyol pathway, in addition to uptake via the fructose transporter GLUT5. Fructose metabolism exacerbates pancreatic cancer proliferation by enhancing glycolysis and accelerating the production of key metabolites that regulate angiogenesis. However, pharmacological blockade of fructose metabolism has been shown to slow pancreatic cancer progression and synergistically enhance anti-tumor capabilities when combined with anti-angiogenic agents. Overall, targeting fructose metabolism may prove to be a promising therapeutic approach in the treatment of pancreatic cancer.

过量的果糖摄入与胰腺癌的发生和进展有关。本研究旨在阐明果糖利用与胰腺癌进展之间的关系。我们的研究结果表明，胰腺癌细胞具有很高的利用果糖的能力，除了通过果糖转运蛋白 GLUT5 摄取外，还能够通过 AKR1B1 介导的多元醇途径将葡萄糖转化为果糖。果糖代谢通过增强糖酵解和加速调节血管生成的关键代谢物的产生来加剧胰腺癌增殖。然而，当与抗血管生成剂联合使用时，果糖代谢的药物阻断已被证明可以减缓胰腺癌的进展并协同增强抗肿瘤能力。总体而言，靶向果糖代谢可能被证明是治疗胰腺癌的一种有前途的治疗方法。