GEO series

Metabolic reprogramming drives pancreatic β cell neogenesis from α cells [ATAC-seq 2]

GSE302787 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2026/06/18 Platform GPL24247

Summary

Loss of functional β cells is a hallmark of diabetes, and restoring β cell mass remains a critical goal in the quest for a specific therapy. One potential strategy is to convert non-β cells in the islet, such as α cells, into insulin-producing cells. Although several compounds have been identified to induce β cell-like features in α cells, none have yet been successfully translated into clinical applications. In this study, we identify PRC2 inhibitors as potent inducers of β cell-enriched gene expression in α cells, acting through modulation of the AR-ETV1 complex. AR inhibition suppresses glycogen synthesis and enhances the pentose phosphate pathway (PPP). Direct metabolic reprogramming with methyl esterified 6-phosphogluconate (ME-6-PG), an intermediate metabolite of the PPP, induces β cell-like features in α cells, stimulate β cell regeneration and ameliorates diabetes. Our findings demonstrate that metabolic reprogramming can drive β cell regeneration and highlight a promising therapeutic strategy for diabetes.

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Also filed as BioProject PRJNA1292172 and SRA study SRP601334. Searching any of these in the dataset finder brings you back here.

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