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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.
Yi et al. (Mon,) studied this question.