ArticleThe Journal of biological chemistry2013
Peroxisome proliferator-activated receptor γ (PPARγ) and its target genes are downstream effectors of FoxO1 protein in islet β-cells: mechanism of β-cell compensation and failure.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Targeting CCR1-mediated macrophage phenotypic switching to alleviate bladder pain and urinary dysfunction in interstitial cystitis.Communications biology · 2026Article
- I-BET151 modulates glucokinase gene expression and beta cell function in part through changes in FOXO1 expression.Diabetologia · 2025Article
- High fat diet exacerbated glycolipid metabolism disorder in kidney Yang deficiency rats by interfering with IRS 1-PI3K (p85) -Akt-GLUT 4 pathway.Lipids in health and disease · 2025Article
- In-vitro antiplatelet effect of melatonin in healthy individuals and patients with type 2 diabetes mellitus.Journal of endocrinological investigation · 2023Article
- The Deficits of Insulin Signal in Alzheimer's Disease and the Mechanisms of Vanadium Compounds in Curing AD.Current issues in molecular biology · 2023Review
- Peroxisomes during postnatal development of mouse endocrine and exocrine pancreas display cell-type- and stage-specific protein composition.Cell and tissue research · 2023Article
- Review
- Quinolinate promotes macrophage-induced immune tolerance in glioblastoma through the NMDAR/PPARγ signaling axis.Nature communications · 2023Article
- Niacin exacerbates β cell lipotoxicity in diet-induced obesity mice through upregulation of GPR109A and PPARγ2: Inhibition by incretin drugs.Frontiers in endocrinology · 2022Article
- SetD7 (Set7/9) is a novel target of PPARγ that promotes the adaptive pancreatic β-cell glycemic response.The Journal of biological chemistry · 2021Article
- Transcriptional mechanisms of pancreatic β-cell maturation and functional adaptation.Trends in endocrinology and metabolism: TEM · 2021Review
- Hypoxylonol F Isolated fromBiomolecules · 2019Article
- Roles of pyruvate carboxylase in human diseases: from diabetes to cancers and infection.Journal of molecular medicine (Berlin, Germany) · 2018Review
- Pair Feeding, but Not Insulin, Phloridzin, or Rosiglitazone Treatment, Curtails Markers of β-Cell Dedifferentiation inDiabetes · 2017Article
- Temporal characterization of β cell-adaptive and -maladaptive mechanisms during chronic high-fat feeding in C57BL/6NTac mice.The Journal of biological chemistry · 2017Article
- Molecular Pharmacology of the Incretin Receptors.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2016Review
- Article
- Article
- FOXO1 content is reduced in cystic fibrosis and increases with IGF-I treatment.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms and signaling pathways that drive islet β-cell compensation and failure are not fully resolved. We have used in vitro and in vivo systems to show that FoxO1, an integrator of metabolic stimuli, inhibits PPARγ expression in β-cells, thus transcription of its target genes (Pdx1, glucose-dependent insulinotropic polypeptide (GIP) receptor, and pyruvate carboxylase) that are important regulators of β-cell function, survival, and compensation. FoxO1 inhibition of target gene transcription is normally relieved when upstream activation induces its translocation from the nucleus to the cytoplasm. Attesting to the central importance of this pathway, islet expression of PPARγ and its target genes was enhanced in nondiabetic insulin-resistant rats and markedly reduced with diabetes induction. Insight into the impaired PPARγ signaling with hyperglycemia was obtained with confocal microscopy of pancreas sections that showed an intense nuclear FoxO1 immunostaining pattern in the β-cells of diabetic rats in contrast to the nuclear and cytoplasmic FoxO1 in nondiabetic rats. These findings suggest a FoxO1/PPARγ-mediated network acting as a core component of β-cell adaptation to metabolic stress, with failure of this response from impaired FoxO1 activation causing or exacerbating diabetes.
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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.