scholarly journals Lithium action on glucose transport in insulin‐resistant rat skeletal muscle: roles of insulin signaling and p38 MAPK

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Antoni Ryszard Macko ◽  
Alan Beneze ◽  
Mary K. Teachey ◽  
Erik J. Henriksen
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
P38 Mapk ◽  
Insulin Signaling ◽  
Rat Skeletal Muscle ◽  
Insulin Resistant

Acute selective glycogen synthase kinase-3 inhibition enhances insulin signaling in prediabetic insulin-resistant rat skeletal muscle

2005 ◽  
Vol 288 (6) ◽  
pp. E1188-E1194 ◽  
Author(s):  
Betsy B. Dokken ◽  
Julie A. Sloniger ◽  
Erik J. Henriksen
Keyword(s):  
Skeletal Muscle ◽  
Tyrosine Phosphorylation ◽  
Glucose Transport ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Glycogen Synthase ◽  
Serine Phosphorylation ◽  
Zucker Rats ◽  
Type I ◽  
Insulin Resistant

Glycogen synthase kinase-3 (GSK3) has been implicated in the multifactorial etiology of skeletal muscle insulin resistance in animal models and in human type 2 diabetic subjects. However, the potential molecular mechanisms involved are not yet fully understood. Therefore, we determined if selective GSK3 inhibition in vitro leads to an improvement in insulin action on glucose transport activity in isolated skeletal muscle of insulin-resistant, prediabetic obese Zucker rats and if these effects of GSK3 inhibition are associated with enhanced insulin signaling. Type I soleus and type IIb epitrochlearis muscles from female obese Zucker rats were incubated in the absence or presence of a selective, small organic GSK3 inhibitor (1 μM CT118637, Ki < 10 nM for GSK3α and GSK3β). Maximal insulin stimulation (5 mU/ml) of glucose transport activity, glycogen synthase activity, and selected insulin-signaling factors [tyrosine phosphorylation of insulin receptor (IR) and IRS-1, IRS-1 associated with p85 subunit of phosphatidylinositol 3-kinase, and serine phosphorylation of Akt and GSK3] were assessed. GSK3 inhibition enhanced ( P <0.05) basal glycogen synthase activity and insulin-stimulated glucose transport in obese epitrochlearis (81 and 24%) and soleus (108 and 20%) muscles. GSK3 inhibition did not modify insulin-stimulated tyrosine phosphorylation of IR β-subunit in either muscle type. However, in obese soleus, GSK3 inhibition enhanced (all P < 0.05) insulin-stimulated IRS-1 tyrosine phosphorylation (45%), IRS-1-associated p85 (72%), Akt1/2 serine phosphorylation (30%), and GSK3β serine phosphorylation (39%). Substantially smaller GSK3 inhibitor-mediated enhancements of insulin action on these insulin signaling factors were observed in obese epitrochlearis. These results indicate that selective GSK3 inhibition enhances insulin action in insulin-resistant skeletal muscle of the prediabetic obese Zucker rat, at least in part by relieving the deleterious effects of GSK3 action on post-IR insulin signaling. These effects of GSK3 inhibition on insulin action are greater in type I muscle than in type IIb muscle from these insulin-resistant animals.

Effects of trandolapril and verapamil on glucose transport in insulin-resistant rat skeletal muscle

Metabolism ◽  
1996 ◽  
Vol 45 (5) ◽  
pp. 535-541 ◽  
Author(s):  
Stephan Jacob ◽  
Erik J. Henriksen ◽  
Donovan L. Fogt ◽  
Günther J. Dietze
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Rat Skeletal Muscle ◽  
Insulin Resistant

Interactions of exercise training and α-lipoic acid on insulin signaling in skeletal muscle of obese Zucker rats

2004 ◽  
Vol 287 (3) ◽  
pp. E529-E536 ◽  
Author(s):  
Vitoon Saengsirisuwan ◽  
Felipe R. Perez ◽  
Julie A. Sloniger ◽  
Thomas Maier ◽  
Erik J. Henriksen
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Glucose Transport ◽  
Soleus Muscle ◽  
Lipoic Acid ◽  
Combination Treatment ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Insulin Resistant

We have shown previously (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ. J Appl Physiol 91: 145–153, 2001) that the antioxidant R-(+)-α-lipoic acid (R-ALA), combined with endurance exercise training (ET), increases glucose transport in insulin-resistant skeletal muscle in an additive fashion. The purpose of the present study was to investigate possible cellular mechanisms responsible for this interactive effect. We evaluated the effects of R-ALA alone, ET alone, or R-ALA and ET in combination on insulin-stimulated glucose transport, protein expression, and functionality of specific insulin-signaling factors in soleus muscle of obese Zucker ( fa/fa) rats. Obese animals remained sedentary, received R-ALA (30 mg·kg body wt−1·day−1), performed ET (daily treadmill running for ≤60 min), or underwent both R-ALA treatment and ET for 15 days. R-ALA or ET individually increased ( P < 0.05) insulin-mediated (5 mU/ml) glucose transport (2-deoxyglucose uptake) in soleus muscle by 45 and 68%, respectively, and this value was increased to the greatest extent (124%) in the combined treatment group. Soleus insulin receptor substrate (IRS)-1 protein was significantly increased by R-ALA alone (30%) or ET alone (31%), and a further enhancement (55%) was observed after the combination treatment in the obese animals. Enhanced levels of IRS-1 protein expression after individual or combined interventions were significantly correlated with insulin action on glucose transport activity ( r = 0.597, P = 0.0055). Similarly, insulin-mediated IRS-1 associated with the p85 regulatory subunit of phosphatidylinositol 3-kinase was increased by R-ALA (317%) and ET (319%) and to the greatest extent (435%) (all P < 0.05) by the combination treatment. These results indicate that the improvements of insulin action in insulin-resistant skeletal muscle after R-ALA or ET, alone and in combination, were associated with increases in IRS-1 protein expression and IRS-1 associated with p85.

Oxidant stress and skeletal muscle glucose transport: Roles of insulin signaling and p38 MAPK

2006 ◽  
Vol 41 (5) ◽  
pp. 818-824 ◽  
Author(s):  
John S. Kim ◽  
Vitoon Saengsirisuwan ◽  
Julie A. Sloniger ◽  
Mary K. Teachey ◽  
Erik J. Henriksen
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
P38 Mapk ◽  
Insulin Signaling ◽  
Oxidant Stress ◽  
Muscle Glucose Transport

O.47 Dissociation of glucose transport and insulin signaling in rat skeletal muscle after trauma

1997 ◽  
Vol 16 ◽  
pp. 13-14
Author(s):  
L. Strömmer ◽  
J.R. Zierath ◽  
C. Koehler ◽  
I. Lundkvist ◽  
H. Wallberg-Henrikssson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Insulin Signaling ◽  
Rat Skeletal Muscle ◽  
O 47
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