scholarly journals The effect of toll-like receptor ligands on energy metabolism and myokine expression and secretion in cultured human skeletal muscle cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ragna H. Tingstad ◽  
Frode Norheim ◽  
Fred Haugen ◽  
Yuan Z. Feng ◽  
Hege S. Tunsjø ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oleic Acid ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Human Skeletal Muscle ◽  
Acid Metabolism ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Metabolic Effects ◽  
Human Skeletal Muscle Cells

AbstractSkeletal muscle plays an important role in glycaemic control and metabolic homeostasis, making it a tissue of interest with respect to type 2 diabetes mellitus. The aim of the present study was to determine if ligands of Toll-like receptors (TLRs) could have an impact on energy metabolism and myokine expression and secretion in cultured human skeletal muscle cells. The myotubes expressed mRNA for TLRs 1–6. TLR3, TLR4, TLR5 and TLR6 ligands (TLRLs) increased glucose metabolism. Furthermore, TLR4L and TLR5L increased oleic acid metabolism. The metabolic effects of TLRLs were not evident until after at least 24 h pre-incubation of the cells and here the metabolic effects were more evident for the metabolism of glucose than oleic acid, with a shift towards effects on oleic acid metabolism after chronic exposure (168 h). However, the stimulatory effect of TLRLs on myokine expression and secretion was detected after only 6 h, where TLR3-6L stimulated secretion of interleukin-6 (IL-6). TLR5L also increased secretion of interleukin-8 (IL-8), while TLR6L also increased secretion of granulocyte–macrophage colony stimulating factor (GM-CSF). Pre-incubation of the myotubes with IL-6 for 24 h increased oleic acid oxidation but had no effect on glucose metabolism. Thus IL-6 did not mimic all the metabolic effects of the TLRLs, implying metabolic effects beyond the actions of this myokine.

Myostatin in relation to physical activity and dysglycaemia and its effect on energy metabolism in human skeletal muscle cells

2015 ◽  
Vol 217 (1) ◽  
pp. 45-60 ◽  
Author(s):  
M. Hjorth ◽  
S. Pourteymour ◽  
S. W. Görgens ◽  
T. M. Langleite ◽  
S. Lee ◽  
...  
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells

Different handling of palmitic acid and oleic acid in human skeletal muscle cells

2011 ◽  
Vol 164 ◽  
pp. S31
Author(s):  
Siril S. Bakke ◽  
Nataša Nikolić ◽  
Cedric Moro ◽  
Line Lauvhaug ◽  
Nina P. Hessvik ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oleic Acid ◽  
Palmitic Acid ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells

scholarly journals Endurance exercise training-responsive miR-19b-3p improves skeletal muscle glucose metabolism

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Julie Massart ◽  
Rasmus J. O. Sjögren ◽  
Brendan Egan ◽  
Christian Garde ◽  
Magnus Lindgren ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Aerobic Exercise Training ◽  
Human Skeletal Muscle Cells

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.

Glucose uptake and metabolism by cultured human skeletal muscle cells: rate-limiting steps

2001 ◽  
Vol 281 (1) ◽  
pp. E72-E80 ◽  
Author(s):  
Laureta M. Perriott ◽  
Tetsuro Kono ◽  
Richard R. Whitesell ◽  
Susan M. Knobel ◽  
David W. Piston ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Glucose Transport ◽  
Human Skeletal Muscle ◽  
Primary Cultures ◽  
Insulin Response ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Insulin Effect ◽  
Human Skeletal Muscle Cells

To use primary cultures of human skeletal muscle cells to establish defects in glucose metabolism that underlie clinical insulin resistance, it is necessary to define the rate-determining steps in glucose metabolism and to improve the insulin response attained in previous studies. We modified experimental conditions to achieve an insulin effect on 3- O-methylglucose transport that was more than twofold over basal. Glucose phosphorylation by hexokinase limits glucose metabolism in these cells, because the apparent Michaelis-Menten constant of coupled glucose transport and phosphorylation is intermediate between that of transport and that of the hexokinase and because rates of 2-deoxyglucose uptake and phosphorylation are less than those of glucose. The latter reflects a preference of hexokinase for glucose over 2-deoxyglucose. Cellular NAD(P)H autofluorescence, measured using two-photon excitation microscopy, is both sensitive to insulin and indicative of additional distal control steps in glucose metabolism. Whereas the predominant effect of insulin in human skeletal muscle cells is to enhance glucose transport, phosphorylation, and steps beyond, it also determines the overall rate of glucose metabolism.

scholarly journals SUN-657 The Effect of Simvastatin on Glucose Metabolism in Primary Human Muscle Cells

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Selina Mäkinen ◽  
Neeta Datta-Sengupta ◽  
Yen Nguyen ◽  
Petro Kyrylenko ◽  
Markku Laakso ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Acid Form ◽  
Lactone Form ◽  
Human Skeletal Muscle Cells ◽  
Glucose Incorporation

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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