Forskolin Inhibits Lipopolysaccharide-Induced Modulation of MCP-1 and GPR120 in 3T3-L1 Adipocytes through an Inhibition of NFB

Figure 8

Data summary. (a) When adipocytes are stimulated with LPS, GPR120 mRNA levels are decreased, while MCP-1 mRNA and protein levels are upregulated via TLR-4 signaling pathway and NFκB activation. (b) When adipocytes are treated with LPS in the presence of FK, the LPS-induced effects on both MCP-1 and GPR120 are inhibited via PKA and CREB activation necessitating CBP binding. AC: adenylyl cyclase; ATP: adenosine triphosphate; cAMP: cyclic adenosine monophosphate; CBP: CREB-binding protein; CREB: cAMP response element-binding protein; FFA: free fatty acids; FK: Forskolin; G-3-P: glycerol-3-phosphate; GK: glycerol kinase; GPR120: G-protein coupled receptor 120; H: catecholamines or hormones; HSL: hormone sensitive lipase; IκBα: inhibitor of kappa B; LPS: lipopolysaccharide; MCP-1: monocyte chemotactic protein-1; NFκB: nuclear factor-κB; p: phosphorylated; PKA: protein kinase A; TAG: triacylglycerol; TLR-4: Toll-like receptor 4.

(a) Response to LPS

(b) Effect of FK on the LPS response