Navegando por Autor "Menezes, Gustavo Batista"

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Acute exercise modulates the inflammatory response in adipose tissue of lean and obese mice.
(2023) Lacerda, Débora Romualdo; Silva, Albená Nunes da; Silveira, Ana Letícia Malheiros; Costa, Kátia Anunciação; Rodrigues, Débora Fernandes; Moraes, Michele Macedo; Pinho, Vanessa; Menezes, Gustavo Batista; Teixeira, Mauro Martins; Wanner, Samuel Penna; Soares, Danusa Dias; Ferreira, Adaliene Versiani Matos
Acute physical exercise act as a metabolic stressor, promoting activation of the immune system, and this response could be relevant in the adipose tissue remodelling process. In addition, some cytokines have important functions in lipolysis. Since chronic exercise improves obesity-related metabolic and inflammatory dysfunction, herein, we investigated the effect of acute exercise on the inflammatory responses in the adipose tissues of lean and obese mice. Lean mice were fed a standard chow diet, whereas obese mice were fed a high- refined carbohydrate (HC) diet for 8 weeks. Both groups were subjected to 60 min of moderately-intensity exercise. In the epididymal adipose tissue (EAT) of lean mice, exercise enhanced IL-6 and TNF-α levels, which correlated positively with increased serum free fatty acid concentrations. In vivo confocal imaging of EAT vessels revealed higher recruitment of neutrophils following exercise. Also, the number of leucocytes expressing CD11b+F480– was elevated 6 h after exercise. Similarly, the CXCL-1 level increased at 6 h and remained high until 24 h after exercise. Myeloperoxidase activity were increased at 6, 12, and 24 h after exercise. Surprisingly, however, no changes were observed in EAT from obese mice considering pro-inflammatory cytokines (IL-6 and TNF-). On the other hand, IL-13, IL-4, and IL-10 levels were higher in obese mice after exercise. These data suggest that acute exercise promotes an inflammatory response in the adipose tissue of lean mice that is observed as part of its role in adipose tissue remodelling. In contrast, acute exercise promotes an anti-inflammatory response in adipose tissue from obese mice, likely as an important tool for restoring homeostatic.
Mechanisms underlying fat pad remodeling induced by fasting : role of PAF receptor.
(2019) Lacerda, Débora Romualdo; Soares, Danusa Dias; Costa, Kátia Anunciação; Silva, Albená Nunes da; Rodrigues, Débora Fernandes; Sabino, Josiana Lopes; Silveira, Ana Letícia Malheiros; Pinho, Vanessa; Vieira, Érica Leandro Marciano; Menezes, Gustavo Batista; Antunes, Maísa Mota; Teixeira, Mauro Martins; Ferreira, Adaliene Versiani Matos
Objectives: Fasting has long been practiced for political and religious reasons and to lose weight. However, biological responses during fasting have yet to be fully understood. Previous studies have shown that cytokines may control fat pad expansion, at least in part, owing to the induction of lipolysis. Indeed, we have previously shown that mice with a lower inflammatory response, such as platelet-activating factor receptor knockout mice (PAFR / ), are prone to gain weight and adiposity. The aims of this study were to determine whether adipose tissue becomes inflamed after fasting and to evaluate whether the PAF signaling is a fator in the fat loss induced by fasting. Methods: Wild-type (WT) and PAFR / mice were fasted for 24 h. Adiposity, leukocyte recruitment, and cytokine levels were evaluated. Multiple comparisons were performed using two-way analysis of variance and post hoc Fisher exact test. Results: After fasting, male WT mice showed lower adiposity (P < 0.001), higher recruitment of immune cells (P < 0.001), and increased cytokine levels (P < 0.05) in adipose tissue. Although WT mice lost ~79% of their adipose tissue mass, PAFR / mice lost only 36%. Additionally, PAFR / mice did not show enhanced cytokine and chemokine levels after fasting (P > 0.05). Conclusion: Despite low-grade inflammation being associated with metabolic syndrome, at least in part, the inflammatory milieu is also important to induce proper fat mobilization and remodeling of adipose tissue.
Role of adipose tissue inflammation in fat pad loss induced by fasting in lean and mildly obese mice.
(2019) Lacerda, Débora Romualdo; Costa, Kátia Anunciação; Silveira, Ana Letícia Malheiros; Rodrigues, Débora Fernandes; Silva, Albená Nunes da; Sabino, Josiana Lopes; Pinho, Vanessa; Menezes, Gustavo Batista; Soares, Danusa Dias; Teixeira, Mauro Martins; Ferreira, Adaliene Versiani Matos
Inflammation induced by obesity contributes to insulin resistance and atherosclerosis. Indeed, high levels of proinflammatory cytokines trigger chronic lowgrade inflammation and promote detrimental metabolic effects in the adipose tissue. On the other hand, inflammation seems to control fat pad expansion and to have important functions on lipolysis and glucose metabolism. Thus, it is possible that inflammation may also drive fat pad loss, as seen during long-fast periods. Herein, we have used fasting as a strategy to induce weight loss and evaluate the possible role of inflammation on adipose tissue remodeling. Male BALB-c mice were fed with chow diet (lean mice) or with high-carbohydrate refined diet (mildly obese mice) for 8 weeks. After that, animals were subjected to 24 h of fasting. There was a 63% reduction of adiposity in lean mice following fasting. Furthermore, the adipose tissue was enriched of immune cells and had a higher content of IL-6, TNF-alpha, IL-10, TGF-β and CXCL-1. Interestingly, mildly obese mice, subjected to the same 24-h fasting period, lost only 33% of their adiposity. Following fasting, these mice did not show any increment in leukocyte recruitment and cytokine levels, as did lean mice. Our findings indicate that inflammation participates in fat mass loss induced by fasting. Although the chronic low-grade inflammation seen in obesity is associated with metabolic diseases, a lower inflammatory response triggered by fasting in mildly obese mice impairs fat pad mobilization.