scholarly journals PGC-1α Is Required for Exercise- and Exercise Training-Induced UCP1 Up-Regulation in Mouse White Adipose Tissue

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64123 ◽  
Author(s):  
Stine Ringholm ◽  
Jakob Grunnet Knudsen ◽  
Lotte Leick ◽  
Anders Lundgaard ◽  
Maja Munk Nielsen ◽  
...  
2013 ◽  
Vol 305 (3) ◽  
pp. E429-E438 ◽  
Author(s):  
Erin J. Stephenson ◽  
Sarah J. Lessard ◽  
Donato A. Rivas ◽  
Matthew J. Watt ◽  
Ben B. Yaspelkis ◽  
...  

Impaired visceral white adipose tissue (WAT) metabolism has been implicated in the pathogenesis of several lifestyle-related disease states, with diminished expression of several WAT mitochondrial genes reported in both insulin-resistant humans and rodents. We have used rat models selectively bred for low- (LCR) or high-intrinsic running capacity (HCR) that present simultaneously with divergent metabolic phenotypes to test the hypothesis that oxidative enzyme expression is reduced in epididymal WAT from LCR animals. Based on this assumption, we further hypothesized that short-term exercise training (6 wk of treadmill running) would ameliorate this deficit. Approximately 22-wk-old rats (generation 22) were studied. In untrained rats, the abundance of mitochondrial respiratory complexes I–V, citrate synthase (CS), and PGC-1 was similar for both phenotypes, although CS activity was greater than 50% in HCR ( P = 0.09). Exercise training increased CS activity in both phenotypes but did not alter mitochondrial protein content. Training increased the expression and phosphorylation of proteins with roles in β-adrenergic signaling, including β3-adrenergic receptor (16% increase in LCR; P < 0.05), NOR1 (24% decrease in LCR, 21% decrease in HCR; P < 0.05), phospho-ATGL (25% increase in HCR; P < 0.05), perilipin (25% increase in HCR; P < 0.05), CGI-58 (15% increase in LCR; P < 0.05), and GLUT4 (16% increase in HCR; P < 0.0001). A training effect was also observed for phospho-p38 MAPK (12% decrease in LCR, 20% decrease in HCR; P < 0.05) and phospho-JNK (29% increase in LCR, 20% increase in HCR; P < 0.05). We conclude that in the LCR-HCR model system, mitochondrial protein expression in WAT is not affected by intrinsic running capacity or exercise training. However, training does induce alterations in the activity and expression of several proteins that are essential to the intracellular regulation of WAT metabolism.


2021 ◽  
Author(s):  
Pasquale Nigro ◽  
Roeland J. W. Middelbeek ◽  
Christiano R. R. Alves ◽  
Susana Rovira–Llopis ◽  
Krithika Ramachandran ◽  
...  

Recent studies demonstrate that adaptations to white adipose tissue are important components of the beneficial effects of exercise training on metabolic health. Exercise training favorably alters the phenotype of subcutaneous inguinal white adipose tissue (iWAT) in male mice including decreasing fat mass, improving mitochondrial function, inducing beiging and stimulating the secretion of adipokines. Here, we find that despite performing more voluntary wheel running compared to males, these adaptations do not occur in the iWAT of female mice. Consistent with sex-specific adaptations, we report that mRNA expression of androgen receptor co-activators are upregulated in iWAT from trained male mice, and that testosterone treatment of primary adipocytes derived from the iWAT of male, but not female mice, phenocopies exercise-induced metabolic adaptations. Sex-specificity also occurs in the secretome profile, as we identify Cysteine Rich Secretory Protein 1(<i>Crisp1</i>) as a novel adipokine that is only secreted from male iWAT in response to exercise. <i>Crisp1</i> expression is upregulated by testosterone and functions to increase glucose and fatty acid uptake. Our finding that adaptations to iWAT with exercise training are dramatically greater in male mice has potential clinical implications for understanding the different metabolic response to exercise training in males and females, and demonstrates the importance of investigating both sexes in studies of adipose tissue biology.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 697-P
Author(s):  
PASQUALE NIGRO ◽  
MARIA VAMVINI ◽  
ROELAND MIDDELBEEK ◽  
MICHAEL F. HIRSHMAN ◽  
LAURIE J. GOODYEAR

Diabetes ◽  
2021 ◽  
pp. db200790
Author(s):  
Pasquale Nigro ◽  
Roeland J. W. Middelbeek ◽  
Christiano R. R. Alves ◽  
Susana Rovira–Llopis ◽  
Krithika Ramachandran ◽  
...  

2010 ◽  
Vol 21 (6) ◽  
pp. e115-e121 ◽  
Author(s):  
D. Hatano ◽  
J. Ogasawara ◽  
S. Endoh ◽  
T. Sakurai ◽  
S. Nomura ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-28 ◽  
Author(s):  
Takuya Sakurai ◽  
Junetsu Ogasawara ◽  
Takako Kizaki ◽  
Shogo Sato ◽  
Yoshinaga Ishibashi ◽  
...  

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-αand 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.


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