GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303297/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE303297GEOGSEfalsePdgfrα deficiency in islet b-cells up-regulates apoptosis 1 of beta-cells and disturbs 2 glucose metabolism in B6 miceWe 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.2026/07/30GSE303297GSM9122934GSM9122933GSM9122936GSM9122935GSM9122937GSM912293234290303297Mus musculus