exercise mimetics
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BMB Reports ◽  
2021 ◽  
Vol 54 (12) ◽  
pp. 581-591
Author(s):  
Young Jin Jang ◽  
Sanguine Byun




2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Masato Iwabu ◽  
Miki Okada-Iwabu ◽  
Hiroaki Tanabe ◽  
Nozomi Ohuchi ◽  
Keiko Miyata ◽  
...  

AbstractAdiponectin receptors, AdipoR1 and AdipoR2 exert anti-diabetic effects. Although muscle-specific disruption of AdipoR1 has been shown to result in decreased insulin sensitivity and decreased exercise endurance, it remains to be determined whether upregulation of AdipoR1 could reverse them in obese diabetic mice. Here, we show that muscle-specific expression of human AdipoR1 increased expression levels of genes involved in mitochondrial biogenesis and oxidative stress-detoxification to almost the same extents as treadmill exercise, and concomitantly increased insulin sensitivity and exercise endurance in obese diabetic mice. Moreover, we created AdipoR-humanized mice which express human AdipoR1 in muscle of AdipoR1·R2 double-knockout mice. Most importantly, the small-molecule AdipoR agonist AdipoRon could exert its beneficial effects in muscle via human AdipoR, and increased insulin sensitivity and exercise endurance in AdipoR-humanized mice. This study suggests that expression of human AdipoR1 in skeletal muscle could be exercise-mimetics, and that AdipoRon could exert its beneficial effects via human AdipoR1.



2019 ◽  
Vol 116 (23) ◽  
pp. 11299-11308 ◽  
Author(s):  
Leonela Amoasii ◽  
Efrain Sanchez-Ortiz ◽  
Teppei Fujikawa ◽  
Joel K. Elmquist ◽  
Rhonda Bassel-Duby ◽  
...  

Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1, and transgenic overexpression of NURR1 in skeletal muscle enhances physical performance in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis, by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism, and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.



2018 ◽  
Vol 138 (10) ◽  
pp. 1285-1290
Author(s):  
Yasuko Manabe
Keyword(s):  


2017 ◽  
Vol 2 (2) ◽  
pp. 153-169 ◽  
Author(s):  
Davide Guerrieri ◽  
Hyo Youl Moon ◽  
Henriette van Praag
Keyword(s):  


2017 ◽  
Vol 25 (2) ◽  
pp. 242-247 ◽  
Author(s):  
Weiwei Fan ◽  
Ronald M. Evans


2016 ◽  
Vol 101 (2) ◽  
pp. 188-190 ◽  
Author(s):  
S Li ◽  
I Laher
Keyword(s):  
Road Map ◽  


2016 ◽  
Vol 57 (1) ◽  
pp. R49-R58 ◽  
Author(s):  
Christopher E Wall ◽  
Ruth T Yu ◽  
Anne R Atkins ◽  
Michael Downes ◽  
Ronald M Evans

Endurance exercise can lead to systemic improvements in insulin sensitivity and metabolic homeostasis, and is an effective approach to combat metabolic diseases. Pharmacological compounds that recapitulate the beneficial effects of exercise, also known as ‘exercise mimetics’, have the potential to improve disease symptoms of metabolic syndrome. These drugs, which can increase energy expenditure, suppress hepatic gluconeogenesis, and induce insulin sensitization, have accordingly been highly scrutinized for their utility in treating metabolic diseases including diabetes. Nevertheless, the identity of an efficacious exercise mimetic still remains elusive. In this review, we highlight several nuclear receptors and cofactors that are putative molecular targets for exercise mimetics, and review recent studies that provide advancements in our mechanistic understanding of how exercise mimetics exert their beneficial effects. We also discuss evidence from clinical trials using these compounds in human subjects to evaluate their efficacy in treating diabetes.



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