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During obesity establishment immune cells resident in adipose tissue become important as sources of pro-inflammatory
mediators. Exercise and caloric restriction are important non-pharmacological tools against body mass increase and
are poorly investigated concerning their effects on immune cells of adipose tissue in obese organisms, especially when a high
fat diet is consumed. Thus, after a previous period of high fat diet consumption, mice were submitted to chronic swimming
training or 30% caloric restriction in order to investigate the effect of both interventions on immune cells resident in adipose
tissue. Our results demonstrated that both exercise and caloric restriction were able to reduce body mass in animals consuming
high fat diet. However, in general, such strategies induced different chances in the numbers of immune cells resident in adipose
tissue or in serum cytokines/chemokines produced by mice in a fat diet regimen. Specifically, exercise was able to increase
NK number in adipose tissue and serum levels of IL-6 and RANTES while caloric restriction increased CD4/CD8 ratio and
increased MCP-1 levels. Together, these data suggest that body mass reduction is not the only prerequisite to determine the
effects of exercise or caloric restriction and reinforce the idea that the combination of both strategies is better than their single
utilization. We also investigated the role of leptin in these parameters using the leptin deficient mice (ob/ob) after swimming
protocol. We observed that exercise didn�t affected the food intake, body weight but modified immune cells of adipose tissue in
ob/ob mice, highlighting the leptin role in exercise and in adipose tissue inflammation.