Exercise training reverses insulin resistance in muscle by enhanced recruitment of GLUT-4 to the cell surface.

  title={Exercise training reverses insulin resistance in muscle by enhanced recruitment of GLUT-4 to the cell surface.},
  author={G. Etgen and J. Jensen and C. Wilson and D. Hunt and S. Cushman and J. Ivy},
  journal={The American journal of physiology},
  volume={272 5 Pt 1},
The effects of exercise training on cell surface GLUT-4 in skeletal muscle of the obese (fa/fa) Zucker rat were investigated using the impermeant glucose transporter photoaffinity reagent 2-N-4-(1-azi-2,2,2-trifluoroethyl)-benzoyl-1,3-bis- (D-mannos-4-yloxy)-2-propylamine (ATB-BMPA). In the absence of insulin, 3-O-methyl-D-glucose transport activity was no different in either fast-twitch (epitrochlearis) or slow-twitch (soleus) muscles of trained and sedentary obese rats. Likewise, basal ATB… Expand
Interactions of exercise training and alpha-lipoic acid on insulin signaling in skeletal muscle of obese Zucker rats.
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. Expand
Exercise training improves muscle insulin resistance but not insulin receptor signaling in obese Zucker rats.
Results are consistent with the hypothesis that, in obese Zucker rats, adaptations occur during training that lead to improved insulin-stimulated muscle glucose uptake without affecting insulin receptor signaling through the PI3-kinase pathway. Expand
Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats.
Results indicate that ET and R-ALA interact in an additive fashion to improve insulin action in insulin-resistant skeletal muscle of the obese Zucker rat. Expand
Resistance training enhances components of the insulin signaling cascade in normal and high-fat-fed rodent skeletal muscle.
It is suggested that resistance training increases insulin-stimulated carbohydrate metabolism in normal skeletal muscle and reverses high-fat diet-induced skeletal muscle insulin resistance by altering components of both the insulin signaling cascade and glucose transporter effector system. Expand
Exercise reverses high-fat diet-induced impairments on compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle.
It is indicated that chronic exercise training, but not rosiglitazone, reverses high-fat diet induced impairments in compartmentalization and activation of components of the insulin-signaling cascade in skeletal muscle. Expand
Exercise maintains euglycemia in association with decreased activation of c-Jun NH2-terminal kinase and serine phosphorylation of IRS-1 in the liver of ZDF rats.
It is shown that, in a rodent model of T2DM, voluntary exercise decreases circulating markers of inflammation and oxidative stress and lowers hepatic JNK activation and Ser(307)-phosphorylated insulin receptor substrate-1, which are associated with decreased hyperglycemia and insulin resistance and reduced expression of the main gluconeogenic enzyme phosphoenolpyruvate carboxykinase. Expand
Effect of insulin and contraction up on glucose transport in skeletal muscle.
The mechanisms involved in the decrease of the amount of GLUT4 translocated to the plasma membrane by altering the exercise-induced enhancement of glucose transport capacity should provide important knowledge to the understanding and managing peripheral insulin resistance. Expand
Exercise training and the antioxidant α-lipoic acid in the treatment of insulin resistance and type 2 diabetes
These studies highlight the effectiveness of combining endurance exercise training and antioxidants in beneficially modulating the molecular defects in insulin action observed in insulin-resistant skeletal muscle. Expand
Effects of exercise training and ACE inhibition on insulin action in rat skeletal muscle.
Results indicate that, in rats with normal insulin sensitivity, exercise training improves oral glucose tolerance and insulin-stimulated muscle glucose transport, whereas ACE inhibition has no effect. Expand
Exercise Effects of Muscle Insulin Signaling and Action
Henriksen, Erik J. Invited Review: Effects of acute exercise and exercise training on insulin resistance. J Appl Physiol 93: 788–796, 2002; 10.1152/japplphysiol.01219.2001.—Insulin resistance ofExpand


Skeletal muscle glucose transport in obese Zucker rats after exercise training.
The results suggest that the improvement in the muscle insulin resistance of the obese Zucker rat after moderate endurance training was associated with an improved in the glucose transport process but that it was fiber-type specific. Expand
Contraction-activated glucose uptake is normal in insulin-resistant muscle of the obese Zucker rat.
The results suggest that maximal skeletal muscle glucose uptake of obese Zucker rats is resistant to stimulation by insulin but not to contractile activity and the relationship between contraction-stimulated glucose uptake and GLUT-4 content appears to be fiber-type specific. Expand
Insulin resistance in obese Zucker rat (fa/fa) skeletal muscle is associated with a failure of glucose transporter translocation.
It is concluded that the insulin resistance of the obese rats involves the failure of translocation of transporters, while the action of insulin to increase the average carrier turnover number is normal. Expand
Insulin resistance in soleus muscle from obese Zucker rats. Involvement of several defective sites.
Several abnormalities are responsible for insulin resistance of muscles from obese Zucker rats among which the authors have observed decreased insulin binding, decreased glucose transport and increased utilization of endogenous fatty acid which could inhibit glucose utilization. Expand
Exercise training increases glucose transporter protein GLUT‐4 in skeletal muscle of obese Zucker (fa/fa) rats
Findings suggest endurance training stimulates expression of skeletal muscle GLUT‐4 protein which may be responsible for the previously observed increase in insulin sensitivity with training. Expand
Identification and Characterization of an Exercise-sensitive Pool of Glucose Transporters in Skeletal Muscle (*)
The separation of the two intracellular GLUT4 pools should be useful in dissecting what are likely to be different signal transduction pathways that mediate their translocation to the cell surface in response to insulin and exercise. Expand
Insulin stimulation of glucose transport activity in rat skeletal muscle: increase in cell surface GLUT4 as assessed by photolabelling.
It is demonstrated that the insulin-stimulated increase in glucose transport activity in skeletal muscle can be accounted for by an increase in surface-accessible GLUT4 content. Expand