Free fatty acid induced impairment of insulin signaling is prevented by the diastereomeric mixture of calophyllic acid and isocalophyllic acid in skeletal muscle cells

2015 ◽  
Vol 746 ◽  
pp. 70-77 ◽  
Author(s):  
Natasha Jaiswal ◽  
Naresh Gunaganti ◽  
Chandan Kumar Maurya ◽  
Tadigoppula Narender ◽  
Akhilesh Kumar Tamrakar
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Insulin Signaling ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Diastereomeric Mixture

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

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.

Effect of Chromium and Zinc on Insulin Signaling in Skeletal Muscle Cells

2004 ◽  
Vol 101 (1) ◽  
pp. 19-36 ◽  
Author(s):  
Edward Roshan Miranda ◽  
Chinmoy Sankar Dey
Keyword(s):  
Skeletal Muscle ◽  
Insulin Signaling ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

Gliclazide increases insulin receptor tyrosine phosphorylation but not p38 phosphorylation in insulin-resistant skeletal muscle cells

2002 ◽  
Vol 205 (23) ◽  
pp. 3739-3746 ◽  
Author(s):  
Naresh Kumar ◽  
Chinmoy S. Dey
Keyword(s):  
Skeletal Muscle ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Tyrosine Phosphorylation ◽  
Insulin Signaling ◽  
Mapk Pathway ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Insulin Resistant ◽  
Resistant Cells

SUMMARY Sulfonylurea drugs are used in the treatment of type 2 diabetes. The mechanism of action of sulfonylureas is to release insulin from pancreatic cells and they have been proposed to act on insulin-sensitive tissues to enhance glucose uptake. The goal of the present study was to test the hypothesis that gliclazide, a second-generation sulfonylurea, could enhance insulin signaling in insulin-resistant skeletal muscle cells. We demonstrated that gliclazide enhanced insulin-stimulated insulin receptor tyrosine phosphorylation in insulin-resistant skeletal muscle cells. Although insulin receptor substrate-1 tyrosine phosphorylation was unaffected by gliclazide treatment, phosphatidylinositol 3-kinase activity was partially restored by treatment with gliclazide. No increase in 2-deoxyglucose uptake in insulin-resistant cells by treatment with gliclazide was observed. Further investigations into the mitogen-activated protein kinase (MAPK) pathway revealed that insulin-stimulated p38 phosphorylation was impaired, as compared with extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinase(JNK), which were phosphorylated normally in insulin-resistant cells. Treatment with gliclazide could not restore p38 phosphorylation in insulin-resistant cells. We propose that gliclazide can regulate part of the insulin signaling in insulin-resistant skeletal muscle, and p38 could be a potential therapeutic target for glucose uptake to treat insulin resistance.

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