Diabetes mellitus and pancreatic ductal adenocarcinoma (PDAC) have a bidirectional relationship in which long-standing type 2 diabetes may contribute to cancer susceptibility, while occult pancreatic cancer may induce new-onset diabetes or worsen pre-existing glycemic control. This narrative review critically synthesizes 18 articles published between 2017 and 2026, including observational studies, systematic reviews, meta-analyses, and narrative reviews. The available evidence supports an association between diabetes and pancreatic cancer, although reverse causality, confounding, and differences in diabetes classification complicate causal interpretation. Recent-onset or rapidly worsening diabetes, particularly when accompanied by unexplained weight loss or pancreatic symptoms, may provide an opportunity for earlier cancer detection. However, existing prediction models require further validation, and diabetes alone does not justify universal pancreatic cancer screening. Proposed biological mechanisms include insulin resistance, hyperinsulinemia, chronic inflammation, and tumor-related endocrine dysfunction, particularly impaired β-cell function. Associations between glucose-lowering medications and pancreatic cancer incidence or survival remain influenced by treatment selection, comparator groups, and methodological biases. Metformin has not been established as an effective strategy for pancreatic cancer prevention or improved survival, while observed associations involving insulin do not demonstrate a causal carcinogenic effect.
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Marraki et al. (2026) studied this question.
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