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 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

Effects of adenosine, exercise, and moderate acute hypoxia on energy substrate utilization of human skeletal muscle

2012 ◽  
Vol 302 (3) ◽  
pp. R385-R390 ◽  
Author(s):  
Ilkka Heinonen ◽  
Jukka Kemppainen ◽  
Kimmo Kaskinoro ◽  
Juha E. Peltonen ◽  
Hannu T. Sipilä ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Acute Hypoxia ◽  
Knee Extension ◽  
Substrate Utilization ◽  
Energy Substrate ◽  
Skeletal Muscle Glucose Uptake ◽  
Knee Extension Exercise

Glucose metabolism increases in hypoxia and can be influenced by endogenous adenosine, but the role of adenosine for regulating glucose metabolism at rest or during exercise in hypoxia has not been elucidated in humans. We studied the effects of exogenous adenosine on human skeletal muscle glucose uptake and other blood energy substrates [free fatty acid (FFA) and lactate] by infusing adenosine into the femoral artery in nine healthy young men. The role of endogenous adenosine was studied by intra-arterial adenosine receptor inhibition (aminophylline) during dynamic one-leg knee extension exercise in normoxia and acute hypoxia corresponding to ∼3,400 m of altitude. Extraction and release of energy substrates were studied by arterial-to-venous (A-V) blood samples, and total uptake or release was determined by the product of A-V differences and muscle nutritive perfusion measured by positron emission tomography. The results showed that glucose uptake increased from a baseline value of 0.2 ± 0.2 to 2.0 ± 2.2 μmol·100 g−1·min−1 during adenosine infusion ( P < 0.05) at rest. Although acute hypoxia enhanced arterial FFA levels, it did not affect muscle substrate utilization at rest. During exercise, glucose uptake was higher (195%) during acute hypoxia compared with normoxia ( P = 0.058), and aminophylline had no effect on energy substrate utilization during exercise, despite that arterial FFA levels were increased. In conclusion, exogenous adenosine at rest and acute moderate hypoxia during low-intensity knee-extension exercise increases skeletal muscle glucose uptake, but the increase in hypoxia appears not to be mediated by adenosine.

scholarly journals Role of reactive oxygen species in contraction-mediated glucose transport in mouse skeletal muscle

2006 ◽  
Vol 575 (1) ◽  
pp. 251-262 ◽  
Author(s):  
Marie E. Sandström ◽  
Shi-Jin Zhang ◽  
Joseph Bruton ◽  
José P. Silva ◽  
Michael B. Reid ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Glucose Transport ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mouse Skeletal Muscle

Insulin-independent glycogen supercompensation in isolated mouse skeletal muscle: role of phosphorylase inactivation

2004 ◽  
Vol 448 (5) ◽  
Author(s):  
MarieE. Sandstr�m ◽  
Fabio Abbate ◽  
DanielC. Andersson ◽  
Shi-Jin Zhang ◽  
H�kan Westerblad ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
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

Role of nitration in control of phosphorylase and glycogenolysis in mouse skeletal muscle

2021 ◽  
Vol 320 (4) ◽  
pp. E691-E701
Author(s):  
Sarah J. Blackwood ◽  
Baptiste Jude ◽  
Theresa Mader ◽  
Johanna T. Lanner ◽  
Abram Katz
Keyword(s):  
Skeletal Muscle ◽  
Redox Control ◽  
Short Term ◽  
Intact Mouse ◽  
Mouse Skeletal Muscle

Here we show that exogenous peroxynitrite results in nitration of phosphorylase as well as inhibition of glycogenolysis in isolated intact mouse skeletal muscle during short-term repeated contractions. However, repeated contractions in the absence of exogenous peroxynitrite do not result in nitration of phosphorylase or affect glycogenolysis, nor does the addition of antioxidants alter glycogenolysis during repeated contractions. Thus phosphorylase is not subject to redox control during repeated contractions.

Abstract 1185: Role Of Sphingosine-1-Phosphate (S1P) In Insulin Signaling.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Suzanne M Nicholl ◽  
Elisa Roztocil ◽  
Mark G Davies
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Receptor Expression ◽  
Serine Phosphorylation ◽  
Glucose Disposal ◽  
Sphingosine 1 Phosphate ◽  
Low Glucose

A failure to increase glucose disposal into peripheral tissues in response to insulin leads to impaired insulin signaling and an inability to uptake glucose leading to the onset of insulin resistance, a major contributing factor to diabetes. We examined the role of sphingosine-1-phosphate (S1P) in insulin signaling and its ability to regulate glucose uptake in skeletal muscle cells. S1P, a sphingolipid found in abundance in the circulation, has been implicated in not only mediating crosstalk with other signaling pathways but has also been implicated in insulin resistance. We hypothesize that S1P interacts with post-receptor insulin signaling to increase glucose disposal in an in vitro model of insulin resistance using differentiated mouse skeletal C2C12 myotubes. Our data demonstrates that S1P (10μM) increases basal glucose levels similar to that observed in response to insulin (100nM) under conditions of low glucose (** p < 0.005: n = 3). Conversely, high glucose conditions completely inhibit both insulin and S1P stimulated glucose uptake (*p < 0.01:n = 3). Pre-incubation with S1P does not augment insulin-induced glucose uptake (***p < 0.001:n = 3), suggesting that S1P does not act via a separate signaling pathway. This is confirmed by our data demonstrating that S1P-induced glucose uptake is abrogated by Cytochalasin B (*p < 0.001:n = 3). In addition, the PI3-K inhibitors, LY294002 and Wortmannin, the Akt inhibitor, AKT2 and the p38MAPK inhibitor, SB203580 significantly inhibited glucose uptake in response to S1P, demonstrating their importance in S1P-induced glucose uptake (*p < 0.05:n = 3). S1P2 and S1P3 receptor expression were upregulated in response to insulin (~2-fold over basal) under low glucose conditions suggesting that insulin may regulate S1P signaling via one or both of these receptors. S1P increased serine phosphorylation of IRS1, both at serine 307 and serines 636/639 maximally after 15 minutes of stimulation. This data has important clinical implications in patients with metabolic syndrome who have impaired skeletal muscle glucose disposal due to insulin resistance and will help guide present and future therapy for patients who have this rapidly growing disease.

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