scholarly journals Circulating Exosomal miR-20b-5p is Elevated in Type 2 Diabetes and Could Impair Insulin Action in Human Skeletal Muscle

Diabetes ◽  
2018 ◽  
pp. db180470 ◽  
Author(s):  
Mutsumi Katayama ◽  
Oscar P.B Wiklander ◽  
Tomas Fritz ◽  
Kenneth Caidahl ◽  
Samir El- Andaloussi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Insulin Action ◽  
Human Skeletal Muscle

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

scholarly journals Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes

Diabetes ◽  
2002 ◽  
Vol 51 (10) ◽  
pp. 2944-2950 ◽  
Author(s):  
D. E. Kelley ◽  
J. He ◽  
E. V. Menshikova ◽  
V. B. Ritov
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Human Skeletal Muscle

scholarly journals Proteome Analysis Reveals Phosphorylation of ATP Synthase β-Subunit in Human Skeletal Muscle and Proteins with Potential Roles in Type 2 Diabetes

2003 ◽  
Vol 278 (12) ◽  
pp. 10436-10442 ◽  
Author(s):  
Kurt Højlund ◽  
Krzysztof Wrzesinski ◽  
Peter Mose Larsen ◽  
Stephen J. Fey ◽  
Peter Roepstorff ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Atp Synthase ◽  
Human Skeletal Muscle ◽  
Proteome Analysis ◽  
Β Subunit

scholarly journals The genetic regulatory signature of type 2 diabetes in human skeletal muscle

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Laura J. Scott ◽  
Michael R. Erdos ◽  
Jeroen R. Huyghe ◽  
Ryan P. Welch ◽  
Andrew T. Beck ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Human Skeletal Muscle

294-LB: Transcriptome-Wide Signals Converge Upon Mitochondrial Function in Developmental Stages of Type 2 Diabetes in Human Skeletal Muscle

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 294-LB
Author(s):  
LUKASZ SZCZERBINSKI ◽  
MAGDALENA NIEMIRA ◽  
KAROL SZCZERBINSKI ◽  
URSZULA PUCHTA ◽  
ELWIRA SIEWIEC ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Human Skeletal Muscle ◽  
Developmental Stages

Direct effects of FGF21 on glucose uptake in human skeletal muscle: implications for type 2 diabetes and obesity

2011 ◽  
Vol 27 (3) ◽  
pp. 286-297 ◽  
Author(s):  
Fredirick L. Mashili ◽  
Reginald L. Austin ◽  
Atul S. Deshmukh ◽  
Tomas Fritz ◽  
Kenneth Caidahl ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Direct Effects ◽  
Diabetes And Obesity

scholarly journals Hyperglycemia, maturity-onset obesity, and insulin resistance in NONcNZO10/LtJ males, a new mouse model of type 2 diabetes

2007 ◽  
Vol 293 (1) ◽  
pp. E327-E336 ◽  
Author(s):  
You-Ree Cho ◽  
Hyo-Jeong Kim ◽  
So-Young Park ◽  
Hwi Jin Ko ◽  
Eun-Gyoung Hong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Mouse Model ◽  
Lipid Content ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Glut4 Expression ◽  
Organ Specific

As a new mouse model of obesity-induced diabetes generated by combining quantitative trait loci from New Zealand Obese (NZO/HlLt) and Nonobese Nondiabetic (NON/LtJ) mice, NONcNZO10/LtJ (RCS10) male mice developed type 2 diabetes characterized by maturity onset obesity, hyperglycemia, and insulin resistance. To metabolically profile the progression to diabetes in preobese and obese states, a 2-h hyperinsulinemic euglycemic clamp was performed and organ-specific changes in insulin action were assessed in awake RCS10 and NON/LtJ (control) males at 8 and 13 wk of age. Prior to development of obesity and attendant increases in hepatic lipid content, 8-wk-old RCS10 mice developed insulin resistance in liver and skeletal muscle due to significant decreases in insulin-stimulated glucose uptake and GLUT4 expression in muscle. Transition to an obese and hyperglycemic state by 13 wk of age exacerbated insulin resistance in skeletal muscle, liver, and heart associated with organ-specific increases in lipid content. Thus, this polygenic mouse model of type 2 diabetes, wherein plasma insulin is only modestly elevated and obesity develops with maturity yet insulin action and glucose metabolism in skeletal muscle and liver are reduced at an early prediabetic age, should provide new insights into the etiology of type 2 diabetes.

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