Effect of exercise training on the density of endothelial cells in the white adipose tissue of rats

Health Promotion Science Group, Department of Human Health Science, Graduate School of Human Health Science, Tokyo Metropolitan University, Hachioji, Japan.
Scandinavian Journal of Medicine and Science in Sports (Impact Factor: 3.17). 12/2011; 21(6):e115-21. DOI: 10.1111/j.1600-0838.2010.01176.x
Source: PubMed

ABSTRACT We examined the effects of a 9-week exercise training (TR) in Wistar male rats, beginning at 4 weeks of age, on the density of endothelial cells (ECs) in epididymal white adipose tissue (WAT) and the mRNA expression of angiogenic factors in adipose tissue stromal vascular fraction (SVF) cells. The number of ECs and mRNA expressions were assessed by lectin staining and real-time reverse transcriptase-polymerase chain reaction, respectively. Compared with control (CR) rats, TR rats gained weight more slowly and had significantly lower final weight of WAT due to the reduction in the size and the number of adipocytes. TR significantly increased the number of ECs per square millimeter and per adipocyte (1.37- and 1.23-fold, respectively) in WAT. This is probably because the number of adipocytes is fewer while the number of ECs is constant in the WAT of TR rats, because the regression line of TR rats for adipocyte number-dependent EC number was shifted toward the left without significant differences in the slopes between groups. TR also induced the upregulation of mRNA expression of vascular endothelial growth factor (Vegf)-A and Vegf-receptor-2 in SVF cells, thereby retaining a constant number of ECs in the WAT.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is recognized as a risk factor for lifestyle-related diseases such as type 2 diabetes and cardiovascular disease. White adipose tissue (WAT) is not only a static storage site for energy; it is also a dynamic tissue that is actively involved in metabolic reactions and produces humoral factors, such as leptin and adiponectin, which are collectively referred to as adipokines. Additionally, because there is much evidence that obesity-induced inflammatory changes in WAT, which is caused by dysregulated expression of inflammation-related adipokines involving tumor necrosis factor- α and monocyte chemoattractant protein 1, contribute to the development of insulin resistance, WAT has attracted special attention as an organ that causes diabetes and other lifestyle-related diseases. Exercise training (TR) not only leads to a decrease in WAT mass but also attenuates obesity-induced dysregulated expression of the inflammation-related adipokines in WAT. Therefore, TR is widely used as a tool for preventing and improving lifestyle-related diseases. This review outlines the impact of TR on the expression and secretory response of adipokines in WAT.
    International Journal of Endocrinology 01/2013; 2013:801743. DOI:10.1155/2013/801743 · 1.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective To investigate the effects of obesity and exercise training on regional adipose tissue angiogenesis and hypoxia markers in rats. Methods Lean (Fa/Fa) and obese (fa/fa) male Zucker rats at 2 months of age were randomly assigned to a sedentary or an exercise training group (lean sedentary: n = 7, lean exercise: n = 8, obese sedentary: n = 7, obese exercise: n = 8). The exercise group walked on a rat treadmill 5 times per week for 8 weeks. Inguinal and epididymal adipose tissue vascular endothelial growth factor A (VEGF-A) and lactate levels were determined. Results There were significant effects of obesity in increasing inguinal (P < 0.001) and epididymal (P < 0.05) adipose tissue VEGF-A, and a significant effect of exercise training in increasing epididymal adipose tissue VEGF-A (P < 0.05). There was a significant effect of obesity in increasing inguinal adipose tissue lactate levels (P < 0.001). Compared to lean sedentary animals, obese sedentary animals had significantly higher epididymal adipose tissue lactate levels (P < 0.001); compared to obese sedentary animals, obese exercise rats had significantly lower epididymal adipose tissue lactate levels (P < 0.05). Conclusions Exercise training increased adipose tissue VEGF-A, an important factor of tissue angiogenesis, and lowered adipose tissue lactate, an indicator of adipose tissue hypoxia in obese rats. However, these effects are depot-specific and only observed in intra-abdominal adipose tissue.
    Metabolism: clinical and experimental 01/2013; DOI:10.1016/j.metabol.2013.12.004 · 3.61 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: As white adipose tissue (WAT) expands under obesogenic conditions, local WAT hypoxia may contribute to the chronic low-grade inflammation observed in obesity. Aerobic exercise training is beneficial in treating WAT inflammation after obesity is established, but it remains unknown whether exercise training, while on a concomitant high-fat (HF) diet, influences WAT inflammation during the development of obesity. We sought to determine the effects of 4, 8, and 12 weeks of HF feeding and/or moderate intensity treadmill exercise training (EX) on the relationship between inflammatory and hypoxic gene expression within mouse WAT. Male C57Bl6/J mice (n = 113) were randomized into low-fat (LF)/sedentary (SED), LF/EX, HF/SED, or HF/EX groups. The low-fat and high-fat diets contained 10% and 60% energy from fat, respectively. Exercise training consisted of treadmill running 5 days/week at 12 m/min, 8% incline, 40 min/day. Quantitative real-time PCR was used to assess gene expression. HF diet impaired glucose regulation, and upregulated WAT gene expression of inflammation (IL-1β, IL-1ra, TNFα), macrophage recruitment and infiltration (F4/80 and monocyte chemoattractant protein), and M1 (CD11c) and M2 (CD206 and Arginase-1) macrophage polarization markers. Treadmill training resulted in a modest reduction of WAT macrophage and inflammatory gene expression. HF diet had little effect on hypoxia-inducible factor-1α and vascular endothelial growth factor, suggesting that WAT inflammatory gene expression may not be driven by hypoxia within the adipocytes. Treadmill training may provide protection by preventing WAT expansion and macrophage recruitment.
    07/2014; 2(7). DOI:10.14814/phy2.12071