<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334569/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334569</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNAseq_Acute Glucose Stimulation Drives Coordinated Translational Reprogramming in Primary Pancreatic Islets: From Global Remodeling to Fine-tuned Insulin Synthesis</name><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.</description><dates><publication>2026/06/15</publication></dates><accession>GSE334569</accession><cross_references><GSM>GSM9791035</GSM><GSM>GSM9791036</GSM><GSM>GSM9791037</GSM><GSM>GSM9791038</GSM><GPL>34290</GPL><GSE>334569</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>