ArticleFrontiers in endocrinology2026
Acute glucose stimulation drives coordinated translational reprogramming in primary pancreatic islets: from global remodeling to fine-tuned insulin synthesis.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pancreatic beta cells must rapidly escalate protein synthesis to maintain systemic glucose homeostasis. While the transcriptional responses are well characterized, the immediate translational dynamics governing this adaptive phase remain poorly defined. Methods: We performed high-resolution ribosome profiling (Ribo-seq) on primary mouse islets under acute low-glucose (2.5 mM) and high-glucose (25 mM) conditions and integrated analysis of the differential translation, functional enrichment, translational efficiency (TE), and ribosome kinetics. The protein levels and mRNA expression were validated using Western blot and quantitative PCR (qPCR), respectively. Results: We identified extensive translational reprogramming involving 1, 680 differentially translated genes. High glucose triggered a significant upregulation of immediate early genes (e.g., Conclusion: Our research characterizes the translatome as a dynamic regulator of the glucose response. By revealing these rapid translational nodes, we provide potential targets to restore the insulin synthetic capacity and secretory function in T2DM, offering a mechanistic framework for the development of therapies centered on preserving β-cell proteostasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.