Trypanosoma cruzi the cause of Chagas disease persists in tissues of infected experimental animals and humans. Here we demonstrate the persistence of the parasite in adipose tissue from of three of 10 elderly seropositive patients with chronic chagasic heart disease. Nine control patients had no parasites in the fat. We also demonstrate that T. cruzi parasitizes primary adipocytes in vitro. Thus, in humans as in mice the parasite may persist in adipose tissue for decades and become a reservoir of infection.

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To investigate the consequences of food allergy in adipose tissue and metabolism, we used a murine model in which mice have been sensitized subcutaneously with ovalbumin and further received antigen-containing diet. Allergic mice presented a significant weight loss 7 days after oral challenge with a concomitant decrease in epididymal adipose tissue mass. This decrease was associated with increased lipolysis and local inflammation. In adipose tissue of allergic mice there were increased leukocyte rolling and adhesion in the microvasculature, increased number of leukocytes in the tissue, especially macrophages (F4/80(+) cells) and increased pro-inflammatory cytokines levels, including TNF-α, IL-6 and CCL2. In addition, we observed low serum concentrations of triglyceride, glucose, total cholesterol and free fatty acids in the allergic mice. Our results suggest that the induction of food allergy in mice leads to adipose tissue inflammation and systemic metabolic alterations that contribute to the weight loss observed.

This study investigated the adipocyte metabolism in wild type (WT) and FVB/N Mas‐deficient male mice (KO). Plasma triglyceride (TG) and free fatty acid (FFA) were assayed by enzymatic methods. Epididymal adipocytes were incubated in the presence or absence of isoproterenol and the effects of insulin on isoproterenol‐stimulated lipolysis were determined. Quantification of hormone‐sensitive lipase (HSL) protein was measured by Western blotting. Epididymal adipocytes were incubated in the presence or absence of insulin and uptake of 2‐deoxy‐[3H] glucose was estimated. Gene expression of PPARγ was measured by real time RT‐PCR. KO mice showed greater levels of plasma TG and FFA compared to WT mice (p<0.05). The lipolitic activity as basal as induced by isoproterenol was the same in both groups. The insulin decreased 41% the lipolitic activities stimulated by isoproterenol in a WT group (p<0.05), while no effect of the insulin action was observed in KO group. The amount of HSL enzyme was similar in WT and KO groups. The glucose uptake in the basal condition was the same in both groups. However, adipocytes of KO group showed a decreasing of 39% of glucose uptake stimulated by insulin compared to adipocytes of WT group (p<0.05). The expression of PPARγ is reduced in 66% in KO animals (p<0.05). Our data suggested that the lack of Ang‐(1‐7) action through Mas receptor alters the response of adipocytes of insulin action.