ArticleAnimal cells and systems2025
RNA binding protein HuD regulates fatty acid oxidation in pancreatic β-cells by modulating long-chain acyl-CoA dehydrogenase expression.
Article in Animal cells and systems, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA binding proteins (RBPs) play crucial roles in the post-transcriptional regulation of metabolic pathways. Although the RBP HuD has been extensively studied in pancreatic β-cells, its role in cellular metabolism remains poorly understood. In this study, we uncover a novel function of HuD in regulating fatty acid oxidation (FAO) in mouse insulinoma βTC6 cells. Through genetic knockdown and overexpression approaches, we demonstrate that HuD modulates the expression of long-chain acyl-CoA dehydrogenase (LCAD), a key enzyme in FAO, by binding to the 3'-untranslated region of its mRNA. Loss of HuD impaired FAO, leading to lipid droplet accumulation, elevated reactive oxygen species production, and increased lipotoxicity under lipid-stress conditions. These findings reveal a previously unrecognized role for HuD in maintaining fatty acid homeostasis and suggest that the HuD-LCAD regulatory axis may represent a promising therapeutic target for preserving β-cell integrity and function.
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.