scholarly journals Aerobic Exercise Training Prevents Perivascular Adipose Tissue-Induced Endothelial Dysfunction in Thoracic Aorta of Obese Mice

2019 ◽  
Vol 10 ◽  
Author(s):  
Andressa S. Sousa ◽  
Amanda C. S. Sponton ◽  
César B. Trifone ◽  
Maria A. Delbin
2017 ◽  
Vol 45 (3) ◽  
pp. 293-302 ◽  
Author(s):  
Hygor N. Araujo ◽  
Jamaira A. Victório ◽  
Carmem P. Valgas da Silva ◽  
Amanda C. S. Sponton ◽  
Jean F. Vettorazzi ◽  
...  

2015 ◽  
Vol 3 (6) ◽  
pp. e12415 ◽  
Author(s):  
R. Grace Walton ◽  
Brian S. Finlin ◽  
Jyothi Mula ◽  
Douglas E. Long ◽  
Beibei Zhu ◽  
...  

2020 ◽  
Vol 319 (3) ◽  
pp. E579-E591 ◽  
Author(s):  
Mariana de Mendonça ◽  
Karina C. Rocha ◽  
Érica de Sousa ◽  
Beatriz M. V. Pereira ◽  
Lila Missae Oyama ◽  
...  

There is a growing body of evidence that extracellular vesicles (EVs) and their cargo of RNA, DNA, and protein are released in the circulation with exercise and might mediate interorgan communication. C57BL6/J male mice were subjected to diet-induced obesity and aerobic training on a treadmill for 8 wk. The effect of aerobic training was evaluated in the liver, muscle, kidney, and white/brown adipose tissue. To provide new mechanistic insight, we profiled miRNA from serum EVs of obese and obese trained mice. We demonstrate that aerobic training changes the circulating EV miRNA profile of obese mice, including decreases in miR-122, miR-192, and miR-22 levels. Circulating miRNA levels were associated with miRNA levels in mouse liver white adipose tissue (WAT). In WAT, aerobically trained obese mice showed reduced adipocyte hypertrophy and increased the number of smaller adipocytes and the expression of Cebpa, Pparg, Fabp4 (adipogenesis markers), and ATP-citrate lyase enzyme activity. Importantly, miR-22 levels negatively correlated with the expression of adipogenesis and insulin sensitivity markers. In the liver, aerobic training reverted obesity-induced steatohepatitis, and steatosis score and Pparg expression were negatively correlated with miR-122 levels. The prometabolic effects of aerobic exercise in obesity possibly involve EV miRNAs, which might be involved in communication between liver and WAT. Our data provide significant evidence demonstrating that aerobic training exercise-induced EVs mediate the effect of exercise on adipose tissue metabolism.


2020 ◽  
Vol 21 (24) ◽  
pp. 9745
Author(s):  
José Cesar Rosa-Neto ◽  
Loreana Sanches Silveira

Adipose tissue is considered an endocrine organ whose complex biology can be explained by the diversity of cell types that compose this tissue. The immune cells found in the stromal portion of adipose tissue play an important role on the modulation of inflammation by adipocytokines secretion. The interactions between metabolic active tissues and immune cells, called immunometabolism, is an important field for discovering new pathways and approaches to treat immunometabolic diseases, such as obesity and cancer. Moreover, physical exercise is widely known as a tool for prevention and adjuvant treatment on metabolic diseases. More specifically, aerobic exercise training is able to increase the energy expenditure, reduce the nutrition overload and modify the profile of adipocytokines and myokines with paracrine and endocrine effects. Therefore, our aim in this review was to cover the effects of aerobic exercise training on the immunometabolism of adipose tissue in obesity and cancer, focusing on the exercise-related modification on adipose tissue or immune cells isolated as well as their interaction.


2017 ◽  
Vol 37 (5) ◽  
pp. 889-899 ◽  
Author(s):  
Joseph Candela ◽  
Rui Wang ◽  
Carl White

Objective— The function of perivascular adipose tissue as an anticontractile mediator in the microvasculature is lost during obesity. Obesity results in inflammation and recruitment of proinflammatory macrophages to the perivascular adipose tissue that is paralleled by depletion of the vasorelaxant signaling molecule hydrogen sulfide (H 2 S) in the vessel. The current objective was to assess the role of macrophages in determining vascular [H 2 S] and defining how this impinged on vasodilation. Approach and Results— Contractility and [H 2 S] were measured in mesenteric resistance arterioles from lean and obese mice by using pressure myography and confocal microscopy, respectively. Vasodilation was impaired and smooth muscle and endothelial [H 2 S] decreased in vessels from obese mice compared with those from lean controls. Coculturing vessels from lean mice with macrophages from obese mice, or macrophage-conditioned media, recapitulated obese phenotypes in vessels. These effects were mediated by low molecular weight species and dependent on macrophage inducible nitric oxide synthase activity. Conclusions— The inducible nitric oxide synthase activity of perivascular adipose tissue–resident proinflammatory macrophages promotes microvascular endothelial dysfunction by reducing the bioavailability of H 2 S in the vessel. These findings support a model in which vascular H 2 S depletion underpins the loss of perivascular adipose tissue anticontractile function in obesity.


2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Anna Laura Viacava Américo ◽  
Cynthia Rodrigues Muller ◽  
Miriam Helena Fonseca‐Alaniz ◽  
Fabiana Sant'Anna Evangelista

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