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Debatri Datta March 11, 2024 Written By Dr

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

The GLP-1 receptor agonists operate via several mechanisms that include increasing glucose-stimulated insulin secretion from the pancreatic beta cells, inhibiting the secretion of inappropriate glucagon in cases where blood glucose is high, slowing down gastric emptying to help control the glucose excursions, and activating brain centers such as the hypothalamus and brain stem to enhance satiety and suppress food intake

At the same time, excess glucose hardens collagen fibers, altering the skin's elasticity