Wolska Waleria, Gutowska Izabela, Wszołek Agata, Żwierełło Wojciech
Department of Medical Chemistry, Pomeranian Medical University in Szczecin, Powstańców Wlkp. 72, 70-111 Szczecin, Poland.
Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Erling Skjalgssons gate 1, 7030 Trondheim, Norway.
Int J Mol Sci. 2025 May 15;26(10):4742. doi: 10.3390/ijms26104742.
Intermittent fasting (IF) is a dietary approach that influences key metabolic pathways, including autophagy-a crucial mechanism in maintaining cellular homeostasis. Autophagy plays a dual role in oncogenesis, acting both as a tumor suppressor and a survival mechanism under metabolic stress. IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy. However, its effects depend heavily on the type and stage of cancer. Potential risks, such as excessive weight loss and malnutrition, require careful evaluation. Further clinical studies are needed to optimize IF protocols as adjuncts to cancer therapy. This review discusses autophagy mechanisms induced by IF, their therapeutic implications in oncology, and the limitations of this dietary strategy.
间歇性禁食（IF）是一种饮食方式，它会影响关键的代谢途径，包括自噬——维持细胞稳态的关键机制。自噬在肿瘤发生过程中发挥双重作用，既是一种肿瘤抑制机制，也是代谢应激下的一种生存机制。间歇性禁食已显示出通过使肿瘤细胞对化疗和放疗敏感来降低癌症风险和提高治疗效果的潜力。然而，其效果在很大程度上取决于癌症的类型和阶段。潜在风险，如过度体重减轻和营养不良，需要仔细评估。需要进一步的临床研究来优化间歇性禁食方案，使其作为癌症治疗的辅助手段。本文综述了间歇性禁食诱导的自噬机制、它们在肿瘤学中的治疗意义以及这种饮食策略的局限性。
