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

scholarly journals Adiponectin improves insulin sensitivity via activation of autophagic flux

2017 ◽  
Vol 59 (4) ◽  
pp. 339-350 ◽  
Author(s):  
Penny Ahlstrom ◽  
Esther Rai ◽  
Suharto Chakma ◽  
Hee Ho Cho ◽  
Palanivel Rengasamy ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Er Stress ◽  
Western Blotting ◽  
Muscle Cells ◽  
Dominant Negative ◽  
Skeletal Muscle Cells ◽  
Dominant Negative Mutant ◽  
Autophagic Flux

Skeletal muscle insulin resistance is known to play an important role in the pathogenesis of diabetes, and one potential causative cellular mechanism is endoplasmic reticulum (ER) stress. Adiponectin mediates anti-diabetic effects via direct metabolic actions and by improving insulin sensitivity, and we recently demonstrated an important role in stimulation of autophagy by adiponectin. However, there is limited knowledge on crosstalk between autophagy and ER stress in skeletal muscle and in particular how they are regulated by adiponectin. Here, we utilized the model of high insulin/glucose (HIHG)-induced insulin resistance, determined by measuring Akt phosphorylation (T308 and S473) and glucose uptake in L6 skeletal muscle cells. HIHG reduced autophagic flux measured by LC3 and p62 Western blotting and tandem fluorescent RFP/GFP-LC3 immunofluorescence (IF). HIHG also induced ER stress assessed by thioflavin T/KDEL IF, pIRE1, pPERK, peIF2α and ATF6 Western blotting and induction of a GRP78-mCherry reporter. Induction of autophagy by adiponectin or rapamycin attenuated HIHG-induced ER stress and improved insulin sensitivity. The functional significance of enhanced autophagy was validated by demonstrating a lack of improved insulin sensitivity in response to adiponectin in autophagy-deficient cells generated by overexpression of dominant negative mutant of Atg5. In summary, adiponectin-induced autophagy in skeletal muscle cells alleviated HIHG-induced ER stress and insulin resistance.

scholarly journals SELENON (SEPN1) protects skeletal muscle from saturated fatty acid-induced ER stress and insulin resistance

Redox Biology ◽  
2019 ◽  
Vol 24 ◽  
pp. 101176 ◽  
Author(s):  
Ersilia Varone ◽  
Diego Pozzer ◽  
Simona Di Modica ◽  
Alexander Chernorudskiy ◽  
Leonardo Nogara ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Er Stress ◽  
Saturated Fatty Acid

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

scholarly journals Nicorandil attenuates high glucose-induced insulin resistance by suppressing oxidative stress-mediated ER stress PERK signaling pathway

2021 ◽  
Vol 9 (1) ◽  
pp. e001884
Author(s):  
Zhongwei Liu ◽  
Haitao Zhu ◽  
Chunhui He ◽  
Ting He ◽  
Shuo Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Protein Kinase ◽  
Glucose Tolerance ◽  
Er Stress ◽  
High Glucose ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

IntroductionGlucose-induced insulin resistance is a typical character of diabetes. Nicorandil is now widely used in ischemic heart disease. Nicorandil shows protective effects against oxidative and endoplasmic reticulum (ER) stress, which are involved in insulin resistance. Here, we investigated mechanisms of nicorandil’s novel pharmacological activity on insulin resistance in diabetes.Research design and methodsNicorandil was administrated to streptozotocin-induced animals with diabetes and high glucose exposed skeletal muscle cells. Insulin resistance and glucose tolerance were evaluated. Molecular mechanisms concerning oxidative stress, ER stress signaling activation and glucose uptake were assessed.ResultsNicorandil attenuated high glucose-induced insulin resistance without affecting fasting blood glucose and glucose tolerance in whole body and skeletal muscle in rats with diabetes. Nicorandil treatment suppressed protein kinase C/nicotinamide adenine dinucleotide phosphate oxidases system activities by reducing cytoplasmic free calcium level in skeletal muscle cells exposed to high glucose. As a result, the oxidative stress-mediated ER stress protein kinase RNA-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2α/activating transcription factor 4/CEBP homologous protein/tribbles homolog (TRB)3 signaling pathway activation was inhibited. Nicorandil downregulated expression of TRB3 and thus facilitated Akt phosphorylation in response to insulin stimulation, leading to glucose transporter4 plasma membrane translocation which promoted glucose uptake capability of skeletal muscle cells.ConclusionsBy reducing cytoplasmic calcium, nicorandil alleviated high glucose-induced insulin resistance by inhibiting oxidative stress-mediated ER stress PERK pathway.

scholarly journals PPARβ/δ prevents endoplasmic reticulum stress-associated inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism

Diabetologia ◽  
2014 ◽  
Vol 57 (10) ◽  
pp. 2126-2135 ◽  
Author(s):  
Laia Salvadó ◽  
Emma Barroso ◽  
Anna Maria Gómez-Foix ◽  
Xavier Palomer ◽  
Liliane Michalik ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Dependent Mechanism

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

Iron Overload Plays an Important Role in ER Stress-Induced Insulin Resistance in Human Skeletal Muscle Cells

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1912-P ◽  
Author(s):  
KWANWOO LEE ◽  
RIHUA CUI ◽  
DAE JUNG KIM ◽  
SUNGE CHOI ◽  
WHA JOUNG LEE ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Iron Overload ◽  
Er Stress ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells
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