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Similarly, exenatide ameliorated the inflammatory response in human RA FLSs by decreasing the oxidative stress capacity of FLSs and down-regulating the expression of IL-1 and IL-6, while suppressing the initiation of p38/MAPK and NF-B signal transduction pathways [240]

Research suggests this dual action creates cellular conditions that favor energy expenditure over energy storage, giving researchers a tool to study metabolic switching mechanisms