FIG. 1.

Obesity significantly reduces levels of the n-3 docosanoid lipid mediator 17-HDHA and PD1 in gonadal adipose tissue. (A) Simplified biosynthetic pathway of EPA- and DHA-derived SPMs and their precursors. (B) Mean body weight of lean (□) and obese mice (■; n = 10 animals per group). Genetically obese animals developed similar obesity compared with WT mice fed a high-fat (HF) diet for 18 weeks (diet-induced obesity). n-3 PUFA–derived 17-HDHA (C), PD1 (D), and 18-HEPE (E) were analyzed in murine gonadal adipose tissue of lean (n = 20 animals per group, pooled for n = 10 samples) and obese mice (n = 10 animals per group) in two different mouse models of obesity using solid-phase extraction and LC-MS/MS. Genetically obese db/db mice were compared with lean db/+ littermates, both fed a normal standard chow, and HF diet-induced obese WT mice were compared with lean WT mice on an LF diet. Lipid mediator concentration of 17-HDHA (F), PD1 (G), and 18-HEPE (H) in gonadal adipose tissue (■) was compared with subcutaneous adipose tissue (▨) of obese db/db and WT HF mice (n = 10 animals per group). All data are mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001. COX-2, cyclooxygenase-2; CYP450, cytochrome P450 enzymes; ND, not detected.