scholarly journals Eicosapentaenoic acid (20:5 n-3) increases fatty acid and glucose uptake in cultured human skeletal muscle cells

2005 ◽  
Vol 47 (2) ◽  
pp. 366-374 ◽  
Author(s):  
Vigdis Aas ◽  
Merethe H. Rokling-Andersen ◽  
Eili Tranheim Kase ◽  
G. Hege Thoresen ◽  
Arild C. Rustan
PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0208048 ◽  
Author(s):  
Nils G. Løvsletten ◽  
Siril S. Bakke ◽  
Eili T. Kase ◽  
D. Margriet Ouwens ◽  
G. Hege Thoresen ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-2
Author(s):  
Nataša Nikolić ◽  
Magdalena Rhedin ◽  
Arild C. Rustan ◽  
Len Storlien ◽  
G. Hege Thoresen ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Julie Massart ◽  
Rasmus J. O. Sjögren ◽  
Brendan Egan ◽  
Christian Garde ◽  
Magnus Lindgren ◽  
...  

AbstractSkeletal muscle is a highly adaptable tissue and remodels in response to exercise training. Using short RNA sequencing, we determine the miRNA profile of skeletal muscle from healthy male volunteers before and after a 14-day aerobic exercise training regime. Among the exercise training-responsive miRNAs identified, miR-19b-3p was selected for further validation. Overexpression of miR-19b-3p in human skeletal muscle cells increases insulin signaling, glucose uptake, and maximal oxygen consumption, recapitulating the adaptive response to aerobic exercise training. Overexpression of miR-19b-3p in mouse flexor digitorum brevis muscle enhances contraction-induced glucose uptake, indicating that miR-19b-3p exerts control on exercise training-induced adaptations in skeletal muscle. Potential targets of miR-19b-3p that are reduced after aerobic exercise training include KIF13A, MAPK6, RNF11, and VPS37A. Amongst these, RNF11 silencing potentiates glucose uptake in human skeletal muscle cells. Collectively, we identify miR-19b-3p as an aerobic exercise training-induced miRNA that regulates skeletal muscle glucose metabolism.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Selina Mäkinen ◽  
Neeta Datta-Sengupta ◽  
Yen Nguyen ◽  
Petro Kyrylenko ◽  
Markku Laakso ◽  
...  

Abstract Statin use, especially treatment with simvastatin, is associated with impaired insulin secretion and whole-body insulin sensitivity, and increased risk for T2D. Here, we investigated the direct effects of lactone- and acid-forms of simvastatin on glucose metabolism in primary human skeletal muscle cells. Exposure of human myotubes to lactone-form simvastatin for 48 h increased glucose uptake and glucose incorporation into glycogen, whereas the acid-form did not affect glucose uptake and decreased glucose incorporation into glycogen. These metabolic actions were accompanied by changes in insulin signaling, as phosphorylation of AS160 and GSK3β was upregulated with lactone-, but not with acid-form simvastatin. Exposure to both lactone and acid-forms of simvastatin led to a decrease in glycolysis and glycolytic capacity, as well as to a decrease in mitochondrial respiration and ATP production. Collectively these data indicate that lactone- and acid forms of simvastatin exhibit differences such that lactone-form increases, and acid-form impairs glucose incorporation into glycogen. Exposure to either form of simvastatin, however, impairs glycolysis and mitochondrial oxidative metabolism in human skeletal muscle cells.


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