scholarly journals Impact of the peroxisome proliferator activated receptor-γ coactivator-1β (PGC-1β) Ala203Pro polymorphism on in vivo metabolism, PGC-1β expression and fibre type composition in human skeletal muscle

Diabetologia ◽  
2007 ◽  
Vol 50 (8) ◽  
pp. 1615-1620 ◽  
Author(s):  
C. Ling ◽  
L. Wegner ◽  
G. Andersen ◽  
P. Almgren ◽  
T. Hansen ◽  
...  
1991 ◽  
Vol 11 (1) ◽  
pp. 41-49 ◽  
Author(s):  
O. Eiken ◽  
C. J. Sundberg ◽  
M. Esbjörnsson ◽  
A. Nygren ◽  
L. Kaijser

1977 ◽  
Vol 52 (3) ◽  
pp. 291-297 ◽  
Author(s):  
R. F. W. Moulds ◽  
A. Young ◽  
D. A. Jones ◽  
R. H. T. Edwards

1. A new method of studying isolated human skeletal muscle has been evaluated. This involves the incubation and electrical stimulation of strips of muscle, obtained at surgical biopsy, that are tied at the cut ends of the fibre bundles. 2. Morphological examination showed that the fibres were sealed off at the cut ends. Damage appeared to be restricted to the areas immediately adjacent to the ties. 3. Contractile properties were well maintained for several hours and measurements of tissue metabolites showed that muscle contents of the high-energy phosphate compounds were well preserved. 4. The isolated preparations were found to have the same contractile properties as human quadriceps femoris studied in vivo by the methods described in the preceding paper. 5. Correlation was found between the relaxation speed of the isolated preparations and their fibre-type composition histochemically determined. 6. It is concluded that this technique is a valid addition to the present methods of studying the physiology and pharmacology of human skeletal muscle.


2007 ◽  
Vol 584 (1) ◽  
pp. 305-312 ◽  
Author(s):  
Anders Rinnov Nielsen ◽  
Remi Mounier ◽  
Peter Plomgaard ◽  
Ole Hartvig Mortensen ◽  
Milena Penkowa ◽  
...  

2006 ◽  
Vol 290 (2) ◽  
pp. E251-E257 ◽  
Author(s):  
Sarah J. Lessard ◽  
Zhi-Ping Chen ◽  
Matthew J. Watt ◽  
Michael Hashem ◽  
Julianne J. Reid ◽  
...  

Rosiglitazone (RSG) is an insulin-sensitizing thiazolidinedione (TZD) that exerts peroxisome proliferator-activated receptor-γ (PPARγ)-dependent and -independent effects. We tested the hypothesis that part of the insulin-sensitizing effect of RSG is mediated through the action of AMP-activated protein kinase (AMPK). First, we determined the effect of acute (30–60 min) incubation of L6 myotubes with RSG on AMPK regulation and palmitate oxidation. Compared with control (DMSO), 200 μM RSG increased ( P < 0.05) AMPKα1 activity and phosphorylation of AMPK (Thr172). In addition, acetyl-CoA carboxylase (Ser218) phosphorylation and palmitate oxidation were increased ( P < 0.05) in these cells. To investigate the effects of chronic RSG treatment on AMPK regulation in skeletal muscle in vivo, obese Zucker rats were randomly allocated into two experimental groups: control and RSG. Lean Zucker rats were treated with vehicle and acted as a control group for obese Zucker rats. Rats were dosed daily for 6 wk with either vehicle (0.5% carboxymethylcellulose, 100 μl/100 g body mass), or 3 mg/kg RSG. AMPKα1 activity was similar in muscle from lean and obese animals and was unaffected by RSG treatment. AMPKα2 activity was ∼25% lower in obese vs. lean animals ( P < 0.05) but was normalized to control values after RSG treatment. ACC phosphorylation was decreased with obesity ( P < 0.05) but restored to the level of lean controls with RSG treatment. Our data demonstrate that RSG restores AMPK signaling in skeletal muscle of insulin-resistant obese Zucker rats.


2020 ◽  
Vol 3 ◽  
pp. 1-10
Author(s):  
Jacob T. Bonafiglia ◽  
Hashim Islam ◽  
Nicholas Preobrazenski ◽  
Patrick Drouin ◽  
Andrew Ma ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nandini Ghosh ◽  
Amitava Das ◽  
Nirupam Biswas ◽  
Surya Gnyawali ◽  
Kanhaiya Singh ◽  
...  

AbstractUrolithin A (UA) is a natural compound that is known to improve muscle function. In this work we sought to evaluate the effect of UA on muscle angiogenesis and identify the underlying molecular mechanisms. C57BL/6 mice were administered with UA (10 mg/body weight) for 12–16 weeks. ATP levels and NAD+ levels were measured using in vivo 31P NMR and HPLC, respectively. UA significantly increased ATP and NAD+ levels in mice skeletal muscle. Unbiased transcriptomics analysis followed by Ingenuity Pathway Analysis (IPA) revealed upregulation of angiogenic pathways upon UA supplementation in murine muscle. The expression of the differentially regulated genes were validated using quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Angiogenic markers such as VEGFA and CDH5 which were blunted in skeletal muscles of 28 week old mice were found to be upregulated upon UA supplementation. Such augmentation of skeletal muscle vascularization was found to be bolstered via Silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator-1-alpha (PGC-1α) pathway. Inhibition of SIRT1 by selisistat EX527 blunted UA-induced angiogenic markers in C2C12 cells. Thus this work provides maiden evidence demonstrating that UA supplementation bolsters skeletal muscle ATP and NAD+ levels causing upregulated angiogenic pathways via a SIRT1-PGC-1α pathway.


2016 ◽  
Vol 41 (8) ◽  
pp. 856-863 ◽  
Author(s):  
Neil A. Schwarz ◽  
Sarah K. McKinley-Barnard ◽  
Mike B. Spillane ◽  
Thomas L. Andre ◽  
Joshua J. Gann ◽  
...  

The purpose of this study was to investigate the acute messenger (mRNA) expression of the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) isoforms, insulin-like growth factor-1Ea (IGF-1Ea), and myostatin in response to 2 resistance exercise intensities. In a uniform-balanced, crossover design, 10 participants performed 2 separate testing sessions involving a lower body resistance exercise component consisting of a lower intensity (50% of 1-repetition maximum; 1RM) protocol and a higher intensity (80% of 1RM) protocol of equal volumes. Muscle samples were obtained at before exercise, 45 min, 3 h, 24 h, and 48 h postexercise. Resistance exercise did not alter total PGC-1α mRNA expression; however, distinct responses of each PGC-1α isoform were observed. The response of each isoform was consistent between sessions, suggesting no effect of resistance exercise intensity on the complex transcriptional expression of the PGC-1α gene. IGF-1Ea mRNA expression significantly increased following the higher intensity session compared with pre-exercise and the lower intensity session. Myostatin mRNA expression was significantly reduced compared with pre-exercise values at all time points with no difference between exercise intensity. Further research is needed to determine the effects of the various isoforms of PGC-1α in human skeletal muscle on the translational level as well as their relation to the expression of IGF-1 and myostatin.


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