{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303297/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE303297"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Pdgfrα deficiency in islet b-cells up-regulates apoptosis 1 of beta-cells and disturbs 2 glucose metabolism in B6 mice","description":"We generated β-cell-specific Pdgfrα-deficient C57BL/6 mice (Pdgfrafl/fl Pdx1-cre+) and assessed their metabolic function on both a normal and a high fat diet. We found that the Pdgfrα-deficient mice gained significantly more body weight, with more body fat, poorer glucose metabolism, and the β-cells were more apoptotic and had lower insulin content. Our further mechanistic investigations showed that Pdgfrα deletion suppressed Atf5 by down regulation of PI3K, leading to enhanced β-cell apoptosis. Atf5 regulates Gadd45b, Bcl2 and aminoacyl-tRNA synthetase expression and alters insulin biosynthesis and glucose metabolism. Targeting these β-cell apoptotic factors may provide an opportunity for improving preventive and/or therapeutic strategies for diabetes and beyond.","dates":{"publication":"2026/07/30"},"accession":"GSE303297","cross_references":{"GSM":["GSM9122934","GSM9122933","GSM9122936","GSM9122935","GSM9122937","GSM9122932"],"GPL":["34290"],"GSE":["303297"],"taxon":["Mus musculus"]}}