Figure 3: Potential molecular targets for reducing inflammation in insulin resistance conditions. Circulated proteins and lipid mediators are included as potential targets. Resolvins, protectins, and maresins are lipid mediators generated from n-3 fatty acid metabolism that have potent anti-inflammatory and immunoregulatory actions, promoting decreased inflammatory cytokine expression. Toll-like receptors (TLRs) are transmembrane receptors that are activated by saturated fatty acids (SFAs) and lipopolysaccharides (LPSs) inducing inflammatory responses. TLRs activate intracellular pathways that inhibit the peroxisome proliferator-activated receptor-γ (PPAR-γ activity). This transcriptional factor is involved with decreased inflammatory cytokine expression and increased Treg cell differentiation. Other cytokines, including tumor necrosis factor-α (TNF-α), also promote PPAR-γ inhibition. G-protein coupled receptor (GPCR) activation may attenuate the production of TNF-α, interleucin-6 (IL-6) and macrophage chemoattractant protein-1. GPR120 is a GPCR activated by n-3 fatty acids in insulin resistance models. COX: cyclooxygenase; IKK: IκB kinase; JNK: c-Jun NH(2)-terminal kinase; PI3 K-γ: phosphatidylinositol 3-kinase-γ; PKC: protein kinase C; PLC-β: phospholipase C-β.