This principle has been extended and refined across diverse targets
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Analysis of pooled data To increase the sample size and BW range, five independent experiments totalling 145 rats were pooled into vehicle (V, n = 38), drug (CS + C + S, n = 57) and calorie restriction (WM + PF, n = 50) groups (Extended Data Table 1)
The anti-inflammatory pathways modulated by GLP-1 receptor activation (NF-kB suppression, macrophage polarization, Treg enhancement) are largely distinct from the pathways targeted by: Methotrexate: Folate metabolism disruption, different anti-inflammatory pathway TNF inhibitors (adalimumab, etanercept): Direct TNF blockade, whereas GLP-1 reduces TNF production upstream IL-6 inhibitors (tocilizumab): Receptor-level blockade, while GLP-1 reduces IL-6 production JAK inhibitors (tofacitinib, baricitinib): Different signaling pathway entirely Corticosteroids: Broad immunosuppression, while GLP-1 is immunomodulatory This pathway complementarity is why additive benefit is biologically plausible
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