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IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition

Figure 3

Anti-hyperphagic response mediated by IL-6.

(A) IL-6 mRNA in the hypothalamus of lean or diet-induced obesity (DIO) rats under resting conditions and lean obese rats immediately after the swimming exercise (SW Exe) or treadmill running (TR Exe). (B) 12 h of food intake in obese rats under resting conditions following intrahypothalamic infusion of different doses of recombinant IL-6. Counter-regulatory effects of anti-IL-6 antibody on food intake in exercised obese rats after (C) insulin or (D) leptin infusion. Western blots of five independent experiments showing hypothalamic lysates from Wistar rats; (E) Expression and activity of protein involved in the inflammatory signaling or ER stress in control animals at rest condition or after acute exercise (F) TLR4 expression, (G) IKKβ phosphorylation, (H) IκBα expression, (I) PERK phosphorylation, (J) CHOP expression, and (K) IRS-1Ser307 phosphorylation from lean, obese, obese injected with recombinant IL-6, obese after exercise, and obese pretreated with anti-IL-6 antibody before the exercise protocol. Data are the means ± SEM. # p<0.05 versus lean group; * p<0.05 versus obese group at rest; ¥ p<0.05 versus respective exercised control rats; ** p<0.01 versus stimulated obese group at rest; § p<0.05 versus obese group injected with recombinant IL-6 and exercised obese rats (n = 8–10 animals per group). Swimming Exercise (SW Exe) or Treadmill Running (TR Exe). Lean animals (white bars) and obese animals (black bars).

Figure 3