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. 2020 Sep 23;11:576347. doi: 10.3389/fimmu.2020.576347

Figure 2.

Figure 2

Schematic depicting interactions between ceramides and inflammatory agonists in adipose tissue. Ceramide accumulation elicits deleterious effects on adipose tissue function by activating Nlrp3 inflammasome that induces inflammation, inhibition of Akt via PKCζ to abrogate insulin signaling, and promoting excessive lipid storage by inhibiting HSL. The immunomodulatory adiponectin exhibits some of its beneficial effects by stimulating ceramidase activity that converts ceramides to sphingosine. Akt, Protein Kinase B; CD-36, cluster of differentiation 36; AdipoR, Adiponectin receptor; CDase, Ceramidase; IKK, Ikappa kinase; IL, interleukin; IR, insulin receptor; LPS, lipopolysaccharide; NF-κB, Nuclear factor kappa-light-chain-enhancer of activated B cells; Nlrp3, NLR family, pyrin domain containing 3; PAI-1, Plasminogen activator inhibitor 1; PKC, protein kinase C; PP2A, Protein phosphatase 2A; sFFA, Saturated fatty acids; TLR4, Toll like receptor-4; TNF-α, Tumor necrosis factor alpha; TNFR, Tumor necrosis factor alpha receptor; uPAR, Urokinase-type plasminogen activator receptor.