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Insulin signaling directly influences immune cell metabolism, macrophage polarization, and T-cell differentiation, thereby shaping inflammatory responses within musculoskeletal tissues ( Increasing evidence from immunometabolic research supports a bidirectional relationship between metabolic dysfunction and inflammatory arthritis, whereby chronic inflammation promotes insulin resistance, which in turn amplifies synovial and entheseal inflammation ( Figure 1 , insulin resistance, adipose tissue inflammation, and impaired incretin signaling converge at the skinjoint axis to amplify IL-23/IL-17driven immune activation and disease progression

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141 This prolonged duration may be driven by albumin binding to the fatty acid residues of GLP-1 RAs and their ability to escape protease metabolism due to amino acid substitutions (Figure 1)

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