scholarly journals Erratum to: Trans Fatty Acid-Induced NF-κB Activation Does Not Induce Insulin Resistance in Cultured Murine Skeletal Muscle Cells

Lipids ◽  
2010 ◽  
Vol 45 (5) ◽  
pp. 463-464
Author(s):  
Pascal P. H. Hommelberg ◽  
Ramon C. J. Langen ◽  
Annemie M. W. J. Schols ◽  
Anon L. M. van Essen ◽  
Frank J. M. Snepvangers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Trans Fatty Acid ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Induce Insulin Resistance ◽  
Murine Skeletal Muscle

Trans Fatty Acid-Induced NF-κB Activation Does Not Induce Insulin Resistance in Cultured Murine Skeletal Muscle Cells

Lipids ◽  
2010 ◽  
Vol 45 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Pascal P. H. Hommelberg ◽  
Ramon C. J. Langen ◽  
Annemie M. W. J. Schols ◽  
Anon L. M. van Essen ◽  
Frank J. M. Snepvangers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Trans Fatty Acid ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Induce Insulin Resistance ◽  
Murine Skeletal Muscle

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

Oleate prevents saturated-fatty-acid-induced ER stress, inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism

Diabetologia ◽  
2013 ◽  
Vol 56 (6) ◽  
pp. 1372-1382 ◽  
Author(s):  
L. Salvadó ◽  
T. Coll ◽  
A. M. Gómez-Foix ◽  
E. Salmerón ◽  
E. Barroso ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Er Stress ◽  
Saturated Fatty Acid ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Dependent Mechanism

4-Hydroxyisoleucine ameliorates fatty acid-induced insulin resistance and inflammatory response in skeletal muscle cells

2014 ◽  
Vol 395 (1-2) ◽  
pp. 51-60 ◽  
Author(s):  
Chandan Kumar Maurya ◽  
Rohit Singh ◽  
Natasha Jaiswal ◽  
K. Venkateswarlu ◽  
Tadigoppula Narender ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Inflammatory Response ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

Fatty acid-induced NF-κB activation and insulin resistance in skeletal muscle are chain length dependent

2009 ◽  
Vol 296 (1) ◽  
pp. E114-E120 ◽  
Author(s):  
Pascal P. H. Hommelberg ◽  
Jogchum Plat ◽  
Ramon C. J. Langen ◽  
Annemie M. W. J. Schols ◽  
Ronald P. Mensink
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Chain Length ◽  
Transcriptional Activity ◽  
Muscle Cells ◽  
Binding Activity ◽  
Skeletal Muscle Cells ◽  
Glut4 Translocation ◽  
L6 Cells

The saturated fatty acid (SFA) palmitate induces insulin resistance in cultured skeletal muscle cells, which may be related to NF-κB activation. The aim of this study was to evaluate whether other SFAs also exert these effects on skeletal muscle and whether these relate to chain length. Therefore, we incubated L6 and C2C12 skeletal muscle cells with four different fatty acids, caprylate (C8:0), laurate (C12:0), palmitate (C16:0), and stearate (C18:0), to study effects on GLUT4 translocation, deoxyglucose uptake, and NF-κB activation. Incubation of L6 cells with the long-chain FAs C16:0 and C18:0 reduced insulin-stimulated GLUT4 translocation and deoxyglucose uptake, whereas L6 cells incubated with the medium-chain FAs C8:0 and C12:0 remained insulin sensitive. Besides increasing NF-κB DNA binding activity in both L6 and C2C12 cells, C16:0 also induced NF-κB transcriptional activity. C18:0 showed comparable effects, whereas the SFAs with shorter chain lengths were not able to elevate NF-κB transcriptional activity. Collectively, these results demonstrate that SFA-induced NF-κB activation coincides with insulin resistance and depends on FA chain length.

scholarly journals Activation of Peroxisome Proliferator-Activated Receptor-δ by GW501516 Prevents Fatty Acid-Induced Nuclear Factor-κB Activation and Insulin Resistance in Skeletal Muscle Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1560-1569 ◽  
Author(s):  
Teresa Coll ◽  
David Álvarez-Guardia ◽  
Emma Barroso ◽  
Anna Maria Gómez-Foix ◽  
Xavier Palomer ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Carnitine Palmitoyltransferase 1

Elevated plasma free fatty acids cause insulin resistance in skeletal muscle through the activation of a chronic inflammatory process. This process involves nuclear factor (NF)-κB activation as a result of diacylglycerol (DAG) accumulation and subsequent protein kinase Cθ (PKCθ) phosphorylation. At present, it is unknown whether peroxisome proliferator-activated receptor-δ (PPARδ) activation prevents fatty acid-induced inflammation and insulin resistance in skeletal muscle cells. In C2C12 skeletal muscle cells, the PPARδ agonist GW501516 prevented phosphorylation of insulin receptor substrate-1 at Ser307 and the inhibition of insulin-stimulated Akt phosphorylation caused by exposure to the saturated fatty acid palmitate. This latter effect was reversed by the PPARδ antagonist GSK0660. Treatment with the PPARδ agonist enhanced the expression of two well known PPARδ target genes involved in fatty acid oxidation, carnitine palmitoyltransferase-1 and pyruvate dehydrogenase kinase 4 and increased the phosphorylation of AMP-activated protein kinase, preventing the reduction in fatty acid oxidation caused by palmitate exposure. In agreement with these changes, GW501516 treatment reversed the increase in DAG and PKCθ activation caused by palmitate. These effects were abolished in the presence of the carnitine palmitoyltransferase-1 inhibitor etomoxir, thereby indicating that increased fatty acid oxidation was involved in the changes observed. Consistent with these findings, PPARδ activation by GW501516 blocked palmitate-induced NF-κB DNA-binding activity. Likewise, drug treatment inhibited the increase in IL-6 expression caused by palmitate in C2C12 and human skeletal muscle cells as well as the protein secretion of this cytokine. These findings indicate that PPARδ attenuates fatty acid-induced NF-κB activation and the subsequent development of insulin resistance in skeletal muscle cells by reducing DAG accumulation. Our results point to PPARδ activation as a pharmacological target to prevent insulin resistance.

Extracts of Hymenocardia acida ameliorate insulin resistance in skeletal muscle cells

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
II Ezeigbo ◽  
C Wheeler-Jones ◽  
S Gibbons ◽  
ME Cleasby
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Ameliorate Insulin Resistance
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