{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334681/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Mus musculus"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334681"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"riboseq_Acute Glucose Stimulation Drives Coordinated Translational Reprogramming in Primary Pancreatic Islets: From Global Remodeling to Fine-tuned Insulin Synthesis","description":"Pancreatic β cells rapidly increase protein synthesis to maintain glucose homeostasis, but the immediate translational dynamics underlying this adaptive response remain poorly defined. In this study, high-resolution ribosome profiling (Ribo-seq) was performed on primary mouse pancreatic islets under acute low-glucose (2.5 mM) and high-glucose (25 mM) conditions. High glucose induced extensive translational reprogramming, including induction of immediate-early genes, suppression of stress-related genes, expansion of the cytosolic translation machinery, coordinated upregulation of secretory pathway components, and metabolic remodeling. Bulk RNA-seq was performed to support translation efficiency analysis. These data define glucose-responsive translational programs in primary islets and provide a resource for understanding β-cell function and insulin synthetic capacity.","dates":{"publication":"2026/06/15"},"accession":"GSE334681","cross_references":{"GSM":["GSM9793170","GSM9793172","GSM9793171","GSM9793174","GSM9793173","GSM9793169"],"GPL":["24247"],"GSE":["334681"],"taxon":["Mus musculus"]}}