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Insulin/IGF-1 signaling: multiple STAT3-related downstream pathways InsR/IGF-1R activate JAK-STAT3 signaling The InsR and IGF-1R proteins are receptor tyrosine kinases (RTK) and thus they are members of the tyrosine kinase superfamily

Palmitate triggers inflammation through TLR4 not by acting as its direct agonist, but by altering cellular metabolism and membrane composition, thereby licensing TLR4-dependent inflammatory responses [36]