ArticleScientific reports2025
Pathogenesis of impaired glucose tolerance in rats based on transcriptome analysis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Transcriptomic Profiling of Diabetic Porcine Wound Healing Model Identifies Key Metabolic, Inflammatory, and Oxidative Stress Pathways.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
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Authors and funding
6 authors.
Funding
Abstract
Impaired glucose tolerance (IGT) is a transitional stage in the development of Type 2 diabetes mellitus (T2DM), but understanding its pathogenesis is currently insufficient. This study established the IGT rats through a high-fat diet combined with intraperitoneal Streptozotocin (STZ) injection to investigate the pathogenesis via transcriptomic profiling of liver tissues. Through transcriptome analysis, a total of 860 up-regulated and 707 down-regulated differentially expressed genes (DEGs) were identified. Enrichment analysis highlighted the PPAR signaling pathway as central to the pathology of IGT. Protein-protein interaction (PPI) network analysis identified IL-1b, Stat1, Igf-1, and Cyp7a1 as Target DEGs (T-DEGs), which were validated by Western blot analysis. Elevated serum levels of IL-6, IFNγ, TNFα, and IL-1β were confirmed via ELISA analysis. The results suggested that signaling pathways such as STAT1/PPARγ/IGF-1, STAT1/PPARγ/Cyp7a1, and STAT1/PPARγ/IL-1β may play crucial roles in the pathogenesis of IGT. These findings provide insight into potential mechanisms and targets for early diagnosis and therapeutic intervention.
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