EFFECT OF FREE FATTY ACID ON EXPRESION OF LIGHT AND HVEM mRNA LEVELS IN CULTURED SKELETAL MUSCLE CELLS

2020 ◽  
Vol 65 (10) ◽  
pp. 108-113
Author(s):  
Hoan Le Ngoc ◽  
Toi Chu Dinh ◽  
Van Ho Thi Hong
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Inflammatory Responses ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Mrna Levels ◽  
Tnf Superfamily ◽  
Herpesvirus Entry Mediator ◽  
Necrosis Factor

Light, tumor necrosis factor superfamily member 14 (TNFSF14), is a secreted peptide of the TNF superfamily. It binds to the herpesvirus entry mediator (HVEM). Light\HVEM signaling is well reported as an important factor linking inflammation and obesity. Here, in the current study, we manipulated skeletal muscle cells incubated in media containing free fatty acid (FFA) to mimic an obesity-related inflammatory environment. Our result revealed that FFA strongly induced expression of mRNA levels of light and interleukin 6 (IL6) - an inflammatory cytokine in the skeletal muscle cells. Surprisingly, expression of HVEM mRNA levels was not significantly different between the FFA-treated skeletal muscle cells and the control cells. These data suggest that FFA increases light expression in skeletal muscle cells that in turn, can bind to HVEM as an autocrine effect inducing inflammatory responses in skeletal muscle cells.

scholarly journals Strawberry extract attenuates glucose and free fatty acid‐mediated impaired insulin signaling in vitro in skeletal muscle cells

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Archana Kangath ◽  
Claire Chang ◽  
Sandhya Krishnankutty ◽  
Ravi Kiran Tadapaneni ◽  
Indika Edirisinghe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Insulin Signaling ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Impaired Insulin

Clove and Its Active Compound Attenuate Free Fatty Acid-Mediated Insulin Resistance in Skeletal Muscle Cells and in Mice

2017 ◽  
Vol 20 (4) ◽  
pp. 335-344 ◽  
Author(s):  
Safina Ghaffar ◽  
Shabbir Khan Afridi ◽  
Meha Fatima Aftab ◽  
Munazza Murtaza ◽  
Rahman M. Hafizur ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Active Compound ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals Palmitate Induces Tumor Necrosis Factor-α Expression in C2C12 Skeletal Muscle Cells by a Mechanism Involving Protein Kinase C and Nuclear Factor-κB Activation

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 552-561 ◽  
Author(s):  
Mireia Jové ◽  
Anna Planavila ◽  
Rosa M. Sánchez ◽  
Manuel Merlos ◽  
Juan Carlos Laguna ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase C ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Kinase C ◽  
Tnf Α ◽  
Fold Induction ◽  
C2c12 Skeletal Muscle Cells

The mechanisms responsible for increased expression of TNF-α in skeletal muscle cells in diabetic states are not well understood. We examined the effects of the saturated acid palmitate on TNF-α expression. Exposure of C2C12 skeletal muscle cells to 0.75 mm palmitate enhanced mRNA (25-fold induction, P < 0.001) and protein (2.5-fold induction) expression of the proinflammatory cytokine TNF-α. This induction was inversely correlated with a fall in GLUT4 mRNA levels (57% reduction, P < 0.001) and glucose uptake (34% reduction, P < 0.001). PD98059 and U0126, inhibitors of the ERK-MAPK cascade, partially prevented the palmitate-induced TNF-α expression. Palmitate increased nuclear factor (NF)-κB activation and incubation of the cells with the NF-κB inhibitors pyrrolidine dithiocarbamate and parthenolide partially prevented TNF-α expression. Incubation of palmitate-treated cells with calphostin C, a strong and specific inhibitor of protein kinase C (PKC), abolished palmitate-induced TNF-α expression, and restored GLUT4 mRNA levels. Palmitate treatment enhanced the expression of phospho-PKCθ, suggesting that this PKC isoform was involved in the changes reported, and coincubation of palmitate-treated cells with the PKC inhibitor chelerythrine prevented the palmitate-induced reduction in the expression of IκBα and insulin-stimulated Akt activation. These findings suggest that enhanced TNF-α expression and GLUT4 down-regulation caused by palmitate are mediated through the PKC activation, confirming that this enzyme may be a target for either the prevention or the treatment of fatty acid-induced insulin resistance.

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