ArticleCell metabolism2025
HNF1A and A1CF coordinate a beta cell transcription-splicing axis that is disrupted in type 2 diabetes.
Article in Cell metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cross-Study Meta-Analysis of Blood Transcriptomes in Type 2 Diabetes.International journal of molecular sciences · 2025Pooled it
- Alterations in Human Milk Adiponectin, Leptin, Resistin, and microRNAs in Mothers With Gestational Diabetes Mellitus Compared With Healthy Controls: A Systematic Review and Network-Based Analysis.Food science & nutrition · 2026Review
- The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.Reviews in endocrine & metabolic disorders · 2026Review
- RNA splicing in health and disease.Molecular biomedicine · 2026Review
- Article
- Donor-matched iPSC model reveals context-dependent T2D genetic signals in fibro-adipogenic progenitors.bioRxiv : the preprint server for biology · 2026Article
- Long non-coding RNAs as molecular links and circulating biomarkers between type 2 diabetes and colorectal cancer: focus on shared signaling pathways, epigenetic regulation, and ubiquitination mechanisms.Frontiers in molecular biosciences · 2026Review
- Latent plasticity of the human pancreas across development, health, and disease.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
22 authors.
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Abstract
Type 2 diabetes (T2D) is a devastating chronic disease marked by pancreatic β cell dysfunction and insulin resistance, whose pathophysiology remains poorly understood. HNF1A, which encodes transcription factor hepatocyte nuclear factor-1 alpha, is the most commonly mutated gene in Mendelian diabetes. HNF1A also carries loss- or gain-of-function coding variants that respectively predispose to or protect against polygenic T2D. The mechanisms underlying HNF1A-deficient diabetes, however, are still unclear. We now demonstrate that diabetes arises from β cell-autonomous defects and identify direct β cell genomic targets of HNF1A. This uncovered a regulatory axis where HNF1A controls transcription of A1CF, which orchestrates an RNA splicing program encompassing genes that regulate β cell function. This HNF1A-A1CF transcription-splicing axis is suppressed in β cells from T2D individuals, while genetic variants reducing pancreatic islet A1CF are associated with increased glycemia and T2D susceptibility. Our findings, therefore, identify a linear hierarchy that coordinates β cell-specific transcription and splicing programs and link this pathway to T2D pathogenesis.
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