Beschreibung:
<jats:title>Abstract</jats:title>
<jats:p>Adipose tissue (AT) inflammation is associated with obesity-induced insulin resistance. Exercise (Exe) prevents the development of chronic inflammatory diseases and insulin resistance largely through unknown mechanisms. We provide data that specialized proresolving lipid mediators (SPM) contribute to the anti-inflammatory effect of Exe. Compared with sedentary controls (Sed), mice exposed to 4 wk of Exe showed elevated AT expression of SPM biosynthetic enzyme Alox15 (Sed 1.12±0.2 vs Exe 1.68±0.1 relative expression, n=5–7), SPM levels (Sed vs Exe; RvD1 156.7±12.0 vs 223.0±24.7; 17R-RvD1 354.0±35.9 vs 534.4±98.9; RvD4 31.31±6.9 vs 123.1±30.7; and 17R-RvD3 2.92±1.1 vs 8.20±1.7 pg/g, n=5–7), and M2 macrophages (F4/80+CD301+; Sed 17.5±3.2 vs Exe 40.9±4.5 %F4/80+, n=4–6). These changes were diet-dependent as high fat (HFD) abrogated this Exe effect in AT when compared with low fat (LFD) controls. The exercise-stimulated Alox15 expression was restricted to AT macrophages (F4/80+ cells; LFD Sed 0.11±0.03 vs LFD Exe 0.23±0.03; HFD Sed 0.10±0.04 vs HFD Exe 0.08±0.02 relative expression, n=3–6), as adipocytes isolated from Exe mice showed no difference compared with Sed controls. That epinephrine (Epi) is released with exercise and stimulates macrophage Alox15 expression and RvD1 production, we questioned if Epi biosynthesis is affected by HFD. HFD feeding diminished expression of phenylethanolamine N-methyltransferase compared with controls (LFD 1.0±0.25 vs HFD 0.36±0.15, n=4). Similarly, obese-diabetic mice (db/db) also showed reduced catecholamine production and biosynthetic enzyme levels. These results suggest that obesity-induced adrenergic dysfunction abrogates exercise-stimulated resolvin production in AT.</jats:p>