{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE302nnn/GSE302889/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE302889"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Metabolic reprogramming drives pancreatic β cell neogenesis from α cells [RNA-Seq 2]","description":"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.","dates":{"publication":"2026/06/18"},"accession":"GSE302889","cross_references":{"GSM":["GSM9112969","GSM9112968","GSM9112967","GSM9112973","GSM9112972","GSM9112971","GSM9112970","GSM9112976","GSM9112975","GSM9112974"],"GPL":["24247"],"GSE":["302889"],"taxon":["Mus musculus"]}}