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Classically, three metabolic alterations have been identified that contribute to the development of T2DM: 1) insulin resistance, 2) an eventual decrease in insulin secretion from pancreatic beta cells, and 3) an excess production of glucose from the liver
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
Finally, we consider factors that could limit the impact of these therapies, outlining reasons why our expectations may not be fully realized
When the receptor for either molecule was removed from the mice, the drug was less effective
