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Abstract
Type 2 diabetes mellitus (T2DM) is associated with interrelated disruptions in gut microbiota, intestinal integrity, immune control, and insulin signaling.
- Reduced levels of butyrate-producing bacteria, such as Faecalibacterium prausnitzii and Roseburia spp., are observed in gut dysbiosis linked to T2DM.
- Opportunistic Gram-negative bacteria proliferate, leading to increased intestinal permeability and translocation of lipopolysaccharide (LPS).
- Activation of the TLR4/MyD88/IKKβ/NF-κB pathway results in heightened production of pro-inflammatory cytokines, which may disrupt insulin signaling.
- Increased oxidative stress and inflammatory damage to β-cells are associated with the activation of the JNK and NLRP3 inflammasome pathways.
- Altered bile acid metabolism could promote insulin resistance and fat accumulation in the liver through disrupted FXR-FGF19 and TGR5-cAMP signaling.
- Dysregulated metabolism of branched-chain amino acids and overactivation of the mTOR/S6K1 pathway may contribute to chronic low-grade inflammation in T2DM.
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