Acute Exercise Induces Phenotypic Switching from M1 to M2 Polarization of Macrophages in White Adipose Tissue of Diet-Induced Obesity Rats
Abstract Number: 147-OR
Authors: ALEXANDRE G. OLIVEIRA, BRUNO M. CARVALHO, DIOZE GUADAGNINI, GUILHERME Z. ROCHA, TIAGO G. ARAUJO, JOSE B. C. CARVALHEIRA, MARIO J. A. SAAD
Institutions: Campinas, Brazil
Results: Macrophages infiltrated in white adipose tissue (WAT) have been identified as an important source of inflammatory cytokine production and a key component in the progression to insulin resistance in a state of obesity. In obese animals, macrophages assume a proinflammatory classical activation profile also known as M1, in contrast to lean conditions with an alternative activation state (M2) and production of immunosuppressive factors, such as IL-10. Although physical exercise might decreases proinflammatory status in WAT, it remains uncertain whether exercise affects the adipocytes or the infiltrated macrophages. Thus the present study aimed to analyze the effects of acute swimming exercise on the inflammatory status and insulin signaling of the tissue fractions, stromal-vascular fraction (SVF) and adipocytes. The effect of exercise was investigated on circulating IL-6 and TNF-α
levels by an enzyme-linked immunosorbent assay, insulin signaling proteins and cytokine production by Western blotting, and also macrophage infiltration and polarization in WAT fractions of diet-induced obesity (DIO). The results showed that acute exercise reduced the proinflammatory status mainly in SVF evidenced by reduced expression of MCP-1, TNF-α and IL-1β, without changing WAT macrophage infiltration. In parallel it also increases the IL-10 and IL-13 protein content. The exercise promotes reduction only in circulating TNF-α levels. We also observed higher insulin-induced phosphorylation of IRβ, IRS-1 and Akt in adipocytes in exercised animals. Our results show that exercise in DIO rats induces not only an important suppression in proinflammatory cytokines, but also increases anti-inflammatory cytokines secretion. Taken together these alterations indicate that the exercise can induces the phenotypic switching from M1 to M2 macrophages and that this condition contributes to exercise-induced improved insulin signaling in WAT of DIO rats.
These data provide considerable progress in our understanding of the molecular events that link physical exercise to an improvement in inflammation and insulin resistance in WAT.