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RNAseq_Acute Glucose Stimulation Drives Coordinated Translational Reprogramming in Primary Pancreatic Islets: From Global Remodeling to Fine-tuned Insulin Synthesis

GSE334569 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2026/06/15 Platform GPL34290
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE334569_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1475481 and SRA study SRP707254. Searching any of these in the dataset finder brings you back here.

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