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. 2018 Dec 13;160(2):293–312. doi: 10.1210/en.2018-00797

Figure 9.

Figure 9.

Lipidomic assessment of proinflammatory lipid mediators and proposed model. (A) Heat map and cluster analysis of Cer species differential by sex in obese male and female GWAT. (B) Relative Cer content, (C) arachidonic acid and arachidic acid content, (D) oleic and linoleic acid content, (E) Fads1 gene expression and Fads2 gene expression, and (F) SCD1 desaturase activity in obese male and female GWAT with and without CL treatment. n = 6 per group. *P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.0001. (G) Proposed model for ADRB3-stimulated lipolysis-induced inflammation. (i) In obese male GWAT, increased insulin levels in obese males leads to inhibition of HSL phosphorylation/activity that impairs the breakdown of DG, thereby facilitating its accumulation. Excess FFA from ADRB3 stimulation may generate aberrant Cer, arachidonic acid (AA) accumulation, causing decreased β-oxidation, and increased inflammatory cytokine (IL-6) production, leading to persistent CD11c+ ATM and CD11c− ATM accumulation and thereby creating a feedback loop between lipid mediators and inflammation. (ii) In obese female GWAT, excess FFA from induced lipolysis leads to elevated p-HSL activity and IL-6 and MCP1 production, but giving rise to less inflammatory lipid mediators such as oleic acid and linoleic acid, leading to CD11c− ATM accumulation and initiating adipose tissue remodeling. DAG, diacylglycerol; F, female; M, male; TAG, triacylglycerol.