ArticleAmerican journal of physiology. Cell physiology2024
Loss of glucose-stimulated β-cell Nr4a1 expression impairs insulin secretion and glucose homeostasis.
Article in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Data mining-based analysis to explore the application of an animal model of diabetic gastroparesis.Frontiers in endocrinology · 2025Pooled it
- Nr4a3 deficiency disrupts MEK1-ERK1/2-Drp1 signaling, driving adiposity and glucose intolerance in male mice.American journal of physiology. Endocrinology and metabolism · 2026Article
- FOXO6 inhibits SMURF2-mediated ubiquitination and degradation of NR4A1 to promote retinal pigment epithelial cell ferroptosis in diabetic retinopathy.Journal of cell communication and signaling · 2026Article
- Review
- Spatial- and Phospho-Proteomic Profiling Reveals Pancreatic and Hepatic Dysfunction in a Rat Model of Lethal Insulin Overdose.International journal of molecular sciences · 2025Article
- Analysis of the differential transcriptome expression profiles during prenatal muscle tissue development in Diqing Tibetan pigs.Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
A central aspect of type 2 diabetes is decreased functional β-cell mass. The orphan nuclear receptor Nr4a1 is critical for fuel utilization, but little is known regarding its regulation and function in the β-cell. Nr4a1 expression is decreased in type 2 diabetes rodent β-cells and type 2 diabetes patient islets. We have shown that Nr4a1-deficient mice have reduced β-cell mass and that Nr4a1 knockdown impairs glucose-stimulated insulin secretion (GSIS) in INS-1 832/13 β-cells. Here, we demonstrate that glucose concentration directly regulates β-cell Nr4a1 expression. We show that 11 mM glucose increases Nr4a1 expression in INS-1 832/13 β-cells and primary mouse islets. We show that glucose functions through the cAMP/PKA/CREB pathway to regulate Nr4a1 mRNA and protein expression. Using
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What Socratic 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 Socratic graph.