scholarly journals Iron overload reduces adiponectin receptor expression via a ROS/FOXO1‐dependent mechanism leading to adiponectin resistance in skeletal muscle cells

2021 ◽  
Author(s):  
Karam Dahyaleh ◽  
Hye K. Sung ◽  
Michelle Prioriello ◽  
Palanivel Rengasamy ◽  
Nhat H. Lam ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Iron Overload ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Skeletal Muscle Cells ◽  
Adiponectin Receptor ◽  
Dependent Mechanism ◽  
Adiponectin Resistance

scholarly journals Hyperglycemia- and hyperinsulinemia-induced alteration of adiponectin receptor expression and adiponectin effects in L6 myoblasts

2005 ◽  
Vol 35 (3) ◽  
pp. 465-476 ◽  
Author(s):  
X Fang ◽  
R Palanivel ◽  
X Zhou ◽  
Y Liu ◽  
A Xu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Cells ◽  
Fatty Acid Uptake ◽  
Receptor Expression ◽  
Skeletal Muscle Cells ◽  
Adiponectin Receptor ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Rat Skeletal Muscle

Adiponectin has been shown to regulate glucose and fatty acid uptake and metabolism in skeletal muscle. Here we investigated the role of the recently cloned adiponectin receptor (AdipoR) isoforms in mediating effects of both globular (gAd) and full-length (fAd) adiponectin, and their regulation by hyperglycemia (25 mM, 20 h) and hyperinsulinemia (100 nM, 20 h). We used L6 rat skeletal muscle cells, which were found to express both AdipoR1 and AdipoR2 mRNA in a ratio of over 6:1 respectively. Hyperglycemia and hyperinsulinemia both decreased AdipoR1 receptor expression by approximately 50%, while the latter induced an increase of approximately threefold in AdipoR2 expression. The ability of gAd to increase GLUT4 myc translocation, glucose uptake, fatty acid uptake and oxidation, as well as AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation, was decreased by both hyperglycemia and hyperinsulinemia. Interestingly, hyperinsulinemia induced the ability of fAd to elicit fatty acid uptake and enhanced fatty acid oxidation in response to fAd. In summary, our results suggest that both hyperglycemia and hyperinsulinemia cause gAd resistance in rat skeletal muscle cells. However, hyperinsulinemia induces a switch toward increased fAd sensitivity in these cells.

ALY688 elicits adiponectin-mimetic signaling and improves insulin action in skeletal muscle cells

2021 ◽  
Author(s):  
Hye Kyoung Sung ◽  
Patricia L. Mitchell ◽  
Sean Gross ◽  
Andre Marette ◽  
Gary Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Muscle Cells ◽  
Temporal Analysis ◽  
Skeletal Muscle Cells ◽  
Adiponectin Receptor ◽  
Metabolic Effects

Adiponectin is well established to mediate many beneficial metabolic effects, and this has stimulated great interest in development and validation of adiponectin receptor agonists as pharmaceutical tools. This study investigated the effects of ALY688, a peptide-based adiponectin receptor agonist, in rat L6 skeletal muscle cells. ALY688 significantly increased phosphorylation of several adiponectin downstream effectors, including AMPK, ACC and p38MAPK, assessed by immunoblotting and immunofluorescence microscopy. Temporal analysis using cells expressing an Akt biosensor demonstrated that ALY688 enhanced insulin sensitivity. This effect was associated with increased insulin-stimulated Akt and IRS-1 phosphorylation. The functional metabolic significance of these signaling effects was examined by measuring glucose uptake in myoblasts stably overexpressing the glucose transporter GLUT4. ALY688 treatment both increased glucose uptake itself and enhanced insulin-stimulated glucose uptake. In the model of high glucose/high insulin (HGHI)-induced insulin resistant cells, both temporal studies using the Akt biosensor as well as immunoblotting assessing Akt and IRS-1 phosphorylation indicated that ALY688 significantly reduced insulin resistance. Importantly, we observed that ALY688 administration to high-fat high sucrose fed mice also improve glucose handling, validating its efficacy in vivo. In summary, these data indicate that ALY688 activates adiponectin signaling pathways in skeletal muscle, leading to improved insulin sensitivity and beneficial metabolic effects.

scholarly journals L-Citrulline Protects Skeletal Muscle Cells from Cachectic Stimuli through an iNOS-Dependent Mechanism

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0141572 ◽  
Author(s):  
Daniel J. Ham ◽  
Benjamin G. Gleeson ◽  
Annabel Chee ◽  
Dale M. Baum ◽  
Marissa K. Caldow ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Dependent Mechanism

scholarly journals Insulin increases mRNA abundance of the amino acid transporter SLC7A5/LAT1 via an mTORC1-dependent mechanism in skeletal muscle cells

2014 ◽  
Vol 2 (3) ◽  
pp. e00238 ◽  
Author(s):  
Dillon K. Walker ◽  
Micah J. Drummond ◽  
Jared M. Dickinson ◽  
Michael S. Borack ◽  
Kristofer Jennings ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amino Acid ◽  
Muscle Cells ◽  
Amino Acid Transporter ◽  
Mrna Abundance ◽  
Skeletal Muscle Cells ◽  
Acid Transporter ◽  
Dependent Mechanism
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