FIG. 7.

17-HDHA treatment increases anti-inflammatory and insulin-sensitizing markers and improves glucose tolerance. Expression of genes encoding PPARγ (Pparg) (A), PPARα (Ppara) (B), GLUT-4 (Slc2a4) (C), and adiponectin (Adipoq) (D) in gonadal adipose tissue after vehicle (VE), DHA, and 17-HDHA treatment of HF-fed WT mice by intraperitoneal injection every 12 h for 8 days (n = 12–14 animals per group). Glucose tolerance test was performed by intraperitoneal injection of 0.75 g 20% glucose/kg body weight (n = 12 animals per group) (E), and plasma insulin concentration was measured at the indicated time points (n = 8 animals per group) (F). Determination of 3-h fasting plasma insulin (n = 10 animals per group) (G), HOMA-IR (n = 10 animals per group) (H), and insulin sensitivity by performing an insulin tolerance test (0.75 units/kg body weight; n = 12 animals per group) (I) upon VE, 17-HDHA, and DHA intraperitoneal injection for 8 days. Three-hour fasting plasma insulin (n = 10 animals per group) (J), HOMA-IR (n = 10 animals per group) (K), insulin sensitivity (n = 14 animals per group) (L), glucose tolerance (n = 12 animals per group) (M), and plasma insulin levels before and in response to glucose tolerance test (n = 6 animals per group) (N) were determined after prolonged 17-HDHA administration for 15 days in WT HF mice by osmotic pumps (body weight: 50.9 ± 0.8 g after VE treatment and 49.5 ± 0.8 g after 17-HDHA treatment). For statistical analysis, DHA- and 17-HDHA–treated animals were compared with the VE-treated control group. All data are mean ± SEM. *P < 0.05; **P < 0.01.