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Interestingly, increased STAT3 signaling exerts a negative feedback response to the function of the JAK-STAT3 signaling pathways, i.e., STAT3 factor induces the expression of SOCS proteins which can interact with and inhibit the function of cytokine receptors and insulin/IGF-1 receptors (Figs

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These disruptions include a reduction in SCFA producers and an increase in bacteria associated with inflammation and metabolic endotoxemia, which may serve as potential biomarkers for disease progression and severity