scholarly journals Chronic hypoxia increases insulin‐stimulated glucose uptake in mouse skeletal muscle

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Jorge Gamboa ◽  
Mary Garcia‐Cazarin ◽  
Francisco Andrade
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Chronic Hypoxia ◽  
Mouse Skeletal Muscle

scholarly journals AS160 Regulates Insulin- and Contraction-stimulated Glucose Uptake in Mouse Skeletal Muscle*

2006 ◽  
Vol 281 (42) ◽  
pp. 31478-31485
Author(s):  
Henning F. Kramer ◽  
Carol A. Witczak ◽  
Eric B. Taylor ◽  
Nobuharu Fujii ◽  
Michael F. Hirshman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Mouse Skeletal Muscle

BRSK1 regulates glucose uptake in L6 cells and mouse skeletal muscle

2013 ◽  
Vol 7 ◽  
pp. e84-e85
Author(s):  
Xu Yan ◽  
Kazuhiro Nakano ◽  
Ding An ◽  
Michael F. Hirshman ◽  
Laurie J. Goodyear
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Mouse Skeletal Muscle ◽  
L6 Cells

scholarly journals Enhancement of Glucose Uptake in Mouse Skeletal Muscle Cells and Adipocytes by P2Y6 Receptor Agonists

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e116203 ◽  
Author(s):  
Ramachandran Balasubramanian ◽  
Bernard Robaye ◽  
Jean-Marie Boeynaems ◽  
Kenneth A. Jacobson
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Mouse Skeletal Muscle ◽  
Receptor Agonists ◽  
P2y6 Receptor

The role of TBC1D1 and TBC1D4 in contraction-induced glucose uptake in mouse skeletal muscle

2015 ◽  
Vol 10 (S 01) ◽  
Author(s):  
C de Wendt ◽  
A Chadt ◽  
J Loffing ◽  
D Loffing-Cueni ◽  
HG Joost ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Mouse Skeletal Muscle

scholarly journals Involvement of the protein kinase Akt2 in insulin-stimulated Rac1 activation leading to glucose uptake in mouse skeletal muscle

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0212219 ◽  
Author(s):  
Nobuyuki Takenaka ◽  
Natsumi Araki ◽  
Takaya Satoh
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Mouse Skeletal Muscle

scholarly journals GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle

Diabetes ◽  
2017 ◽  
Vol 66 (6) ◽  
pp. 1491-1500 ◽  
Author(s):  
Shawna L. McMillin ◽  
Denise L. Schmidt ◽  
Barbara B. Kahn ◽  
Carol A. Witczak
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Hypertrophic Growth ◽  
Mouse Skeletal Muscle

Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise

2006 ◽  
Vol 101 (5) ◽  
pp. 1368-1376 ◽  
Author(s):  
Taku Hamada ◽  
Edward B. Arias ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Genetically Modified ◽  
Extensor Digitorum ◽  
Exercise Protocol ◽  
Mouse Skeletal Muscle ◽  
Prior Exercise

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 μU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation ( P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased ( P < 0.05) ∼85 min after exercise in the epitrochlearis (sedentary: 0.266 ± 0.045 μmol·g−1·15 min−1; exercised: 0.414 ± 0.051) and soleus (sedentary: 0.102 ± 0.049; exercised: 0.347 ± 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.

Possible CaMKK-dependent regulation of AMPK phosphorylation and glucose uptake at the onset of mild tetanic skeletal muscle contraction

2007 ◽  
Vol 292 (5) ◽  
pp. E1308-E1317 ◽  
Author(s):  
Thomas E. Jensen ◽  
Adam J. Rose ◽  
Sebastian B. Jørgensen ◽  
Nina Brandt ◽  
Peter Schjerling ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Competitive Inhibitor ◽  
Independent Effect ◽  
Tetanic Contraction ◽  
Mouse Skeletal Muscle ◽  
Ampk Phosphorylation ◽  
Dependent Protein

The Ca2+/calmodulin (CaM) competitive inhibitor KN-93 has previously been used to evaluate 5′-AMP-activated protein kinase (AMPK)-independent Ca2+-signaling to contraction-stimulated glucose uptake in muscle during intense electrical stimulation ex vivo. With the use of low-intensity tetanic contraction of mouse soleus and extensor digitorum longus (EDL) muscles ex vivo, this study demonstrates that KN-93 can potently inhibit AMPK phosphorylation and activity after 2 min but not 10 min of contraction while strongly inhibiting contraction-stimulated 2-deoxyglucose uptake at both the 2- and 10-min time points. These data suggest inhibition of Ca2+/CaM-dependent signaling events upstream of AMPK, the most likely candidate being the novel AMPK kinase CaM-dependent protein kinase kinase (CaMKK). CaMKK protein expression was detected in mouse skeletal muscle. Similar to KN-93, the CaMKK inhibitor STO-609 strongly reduced AMPK phosphorylation and activity at 2 min and less potently at 10 min. Pretreatment with STO-609 inhibited contraction-stimulated glucose uptake at 2 min in soleus, but not EDL, and in both muscles after 10 min. Neither KN-93 nor STO-609 inhibited 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside-stimulated glucose uptake, AMPK phosphorylation, or recombinant LKB1 activity, suggestive of an LKB1-independent effect. Finally, neither KN-93 nor STO-609 had effects on the reductions in glucose uptake seen in mice overexpressing a kinase-dead AMPK construct, indicating that the effects of KN-93 and STO-609 on glucose uptake require inhibition of AMPK activity. We propose that CaMKKs act in mouse skeletal muscle regulating AMPK phosphorylation and glucose uptake at the onset of mild tetanic contraction and that an intensity- and/or time-dependent switch occurs in the relative importance of AMPKKs during contraction.

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