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Pancreatic ductal adenocarcinoma (PDAC) is frequently associated with new-onset diabetes (NOD) in adults aged ≥ 50 years. Accordingly, NOD may serve as an early clinical marker for PDAC, although the causal links remain incompletely defined. This review synthesises clinical and experimental evidence into an islet-centric view in which tumour-derived signals and microenvironmental changes impair β-cell insulin secretion and disrupt α- and δ-cell regulation. We distinguish findings established in PDAC from mechanisms inferred from islet physiology and systemic metabolism. Key uncertainties include the timing of systemic versus local drivers, the clinical relevance of tumour-derived signals in driving dysglycaemia, the status of endocrine cell signalling and endocrine-exocrine crosstalk, and the effects of microvascular and matrix changes on endocrine-vascular exchange. This synthesis highlights mechanisms that remain incompletely defined and prioritises areas for further research.

More information Original publication

DOI

10.3390/ijms262110245

Type

Journal article

Publication Date

2025-10-22T00:00:00+00:00

Volume

26

Keywords

PDAC, diabetes, new-onset diabetes, type 3c diabetes, Humans, Pancreatic Neoplasms, Diabetes Mellitus, Carcinoma, Pancreatic Ductal, Animals, Tumor Microenvironment, Insulin-Secreting Cells, Islets of Langerhans, Insulin