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Mechanism of Action: IGF-1 LR3 vs IGF-1 DES Both IGF-1 LR3 and IGF-1 DES bind to the IGF-1 receptor , triggering powerful anabolic pathwaysprimarily PI3K/Akt/mTOR for muscle protein synthesis and MAPK for cell proliferation

Consistent with this prediction, there is little discernible difference in the [RSSH]-dependence of the rate of O2-consumption between the two substrates (Fig

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It inhibited NO, PGE-2 and proinflammatory cytokines (TNF-, IL-1 and IL-6) while reducing ROS production and NADPH oxidase activation