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Effect on inflammation modulation of adipose tissue of obese mice by physical training


Obesity is a worldwide epidemy and it is related with increase of prevalence highlights the demographic, socio economic and epidemiological transition that led to a decrease in nutritional patterns and physical activity. This disease is associated with subclinical inflammation, characterized by abnormal production of proinflammatory cytokines. Various cells such as adipocytes and macrophages, are involved in this irregular pattern of cytokines which prevents proper intracellular signaling of insulin providing the state of insulin resistance and the onset of Diabetes type II. Is well established that physical exercise as a model measurable stress induction causes functional changes in the immune system. However, little is known about the exercise as a stimulator of macrophages and its effects on immune modulation of diseases related to obesity. From these data we aimed to assess the role of physical exercise on the inflammatory response of adipose tissue of mice subjected to high fat diet. To demonstrate this phenomenon, animals fed a control diet or high fat diet will be submitted for two swimming protocols: the first group will training for 15 minutes daily in an attempt not weight loss and a second will swim for 60 minutes a day where we expect a decrease in adiposity. Another group of animals fed a high fat diet will undergo a food restriction of 40% to compare with the group exercised for 60 minutes. Will be evaluated by flow cytometry the number of CD4 +, CD8 +, neutrophils and macrophages in inguinal adipose tissue. The tissue concentration and plasma adipokines 17 pro or anti-inflammatory will be evaluated using the test bioplex. It will be also assessed insulin resistance by the glucose tolerance test and insulin and blood lipid parameters before and after intervention. To estimate the role of leptin in adipose tissue inflammation and in response to exercise animals deficient for leptin (ob / ob) will be subject to the same procedures described above. (AU)

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Scientific publications (5)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ROSA, T. S.; AMORIM, C. E. N.; BARROS, C. C.; HARO, A. S.; WASINSKI, F.; RUSSO, F. J.; BACURAU, R. F. P.; ARAUJO, R. C. Role of leptin in body temperature regulation and lipid metabolism following splenectomy. Neuropeptides, v. 54, p. 67-72, DEC 2015. Web of Science Citations: 3.
ESTRELA, GABRIEL R.; WASINSKI, FREDERICK; BACURAU, REURY F.; MALHEIROS, DENISE M. A. C.; CAMARA, NIELS O. S.; ARAUJO, RONALDO C. Kinin B-2 receptor deletion and blockage ameliorates cisplatin-induced acute renal injury. International Immunopharmacology, v. 22, n. 1, p. 115-119, SEP 2014. Web of Science Citations: 4.
ESTRELA, GABRIEL R.; WASINSKI, FREDERICK; ALMEIDA, DANILO C.; AMANO, MARIANE T.; CASTOLDI, ANGELA; DIAS, CAROLINA C.; MALHEIROS, DENISE M. A. C.; ALMEIDA, SANDRO S.; PAREDES-GAMERO, EDGAR J.; PESQUERO, JOAO B.; BARROS, CARLOS C.; CAMARA, NIELS O. S.; ARAUJO, RONALDO C. Kinin B1 receptor deficiency attenuates cisplatin-induced acute kidney injury by modulating immune cell migration. JOURNAL OF MOLECULAR MEDICINE-JMM, v. 92, n. 4, p. 399-409, APR 2014. Web of Science Citations: 6.
VIEIRA OLHER, RAFAEL DOS REIS; BOCALINI, DANILO SALES; BACURAU, REURY FRANK; RODRIGUEZ, DANIEL; FIGUEIRA, JR., AYLTON; PONTES, JR., FRANCISCO LUCIANO; NAVARRO, FRANCISCO; SIMOES, HERBERT GUSTAVO; ARAUJO, RONALDO CARVALHO; MORAES, MILTON ROCHA. Isometric handgrip does not elicit cardiovascular overload or post-exercise hypotension in hypertensive older women. CLINICAL INTERVENTIONS IN AGING, v. 8, p. 649-655, 2013. Web of Science Citations: 18.
WASINSKI, FREDERICK; BACURAU, REURY F. P.; MORAES, MILTON R.; HARO, ANDERSON S.; MORAES-VIEIRA, PEDRO M. M.; ESTRELA, GABRIEL R.; PAREDES-GAMERO, EDGAR J.; BARROS, CARLOS C.; ALMEIDA, SANDRO S.; CAMARA, NIELS O. S.; ARAUJO, RONALDO C. Exercise and Caloric Restriction Alter the Immune System of Mice Submitted to a High-Fat Diet. Mediators of Inflammation, 2013. Web of Science Citations: 19.

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