The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation.

@article{Konrad2001TheAD,
  title={The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation.},
  author={Daniel Konrad and Romel Somwar and Gary Sweeney and Karen Yaworsky and Michi Hayashi and Toolsie Ramlal and Amira Klip},
  journal={Diabetes},
  year={2001},
  volume={50 6},
  pages={
          1464-71
        }
}
The cofactor of mitochondrial dehydrogenase complexes and potent antioxidant alpha-lipoic acid has been shown to lower blood glucose in diabetic animals. alpha-Lipoic acid enhances glucose uptake and GLUT1 and GLUT4 translocation in 3T3-L1 adipocytes and L6 myotubes, mimicking insulin action. In both cell types, insulin-stimulated glucose uptake is reduced by inhibitors of p38 mitogen-activated protein kinase (MAPK). Here we explore the effect of alpha-lipoic acid on p38 MAPK… 
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α-Lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes
Need for GLUT4 activation to reach maximum effect of insulin-mediated glucose uptake in brown adipocytes isolated from GLUT4myc-expressing mice.
TLDR
TheGLUT4myc mouse is a promising model for measuring GLUT4 translocation in intact primary cells and affords direct comparison between GLUT 4 translocation and glucose uptake in similar cell preparations, allowing one to study the regulation of GLut4 activity.
The AMP-activated protein kinase activator AICAR does not induce GLUT 4 translocation to transverse tubules but stimulates glucose uptake and p 38 mitogen-activated protein kinases and in skeletal muscle
TLDR
The results suggest that AICAR increases muscle glucose uptake by two mechanisms: 1) inducing selective recruitment of GLUT4 to the plasma membrane, and 2) activating p38 MAPK and , which may be involved in the activation ofGLUT4.
Need for GLUT 4 Activation to Reach Maximum Effect of Insulin-Mediated Glucose Uptake in Brown Adipocytes Isolated From GLUT 4 myc-Expressing Mice
TLDR
TheGLUT4myc mouse is a promising model for measuring GLUT4 translocation in intact primary cells and affords direct comparison between GLUT 4 translocation and glucose uptake in similar cell preparations, allowing one to study the regulation of GLUT3 activity.
The AMP‐activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen‐activated protein kinases α and β in skeletal muscle
TLDR
The results suggest that AICAR increases muscle glucose uptake by two mechanisms: 1) inducing selective recruitment of GLUT4 to the plasma membrane, and 2) activating p38 MAPKα and β, which may be involved in the activation ofGLUT4.
Capsaicin stimulates glucose uptake in C2C12 muscle cells via the reactive oxygen species (ROS)/AMPK/p38 MAPK pathway.
R-α-Lipoic Acid Action on Cell Redox Status, the Insulin Receptor, and Glucose Uptake in 3T3-L1 Adipocytes
TLDR
3T3-L1 adipocytes have a low capacity to reduce R-LA and the oxidized form of lipoic acid is responsible for stimulating glucose up- take, and the insulin re- ceptor is a potential cellular target for R- LA action.
α-Lipoic acid regulates AMP-activated protein kinase and inhibits insulin secretion from beta cells
TLDR
This study is the first to demonstrate that α-LA directly affects beta cell function, and the chronic effects ofα-LA include AMPK activation and reductions in insulin secretion and content, and cell growth.
Utilization of the insulin-signaling network in the metabolic actions of alpha-lipoic acid-reduction or oxidation?
  • D. Konrad
  • Biology
    Antioxidants & redox signaling
  • 2005
TLDR
Given the potential role of oxidative stress in the pathogenesis of secondary complications in diabetes, alpha-lipoic acid might be beneficial in the prevention/treatment of these complications as was recently shown for diabetic neuropathy.
Rosiglitazone produces insulin sensitisation by increasing expression of the insulin receptor and its tyrosine kinase activity in brown adipocytes
TLDR
At the insulin receptor level, rosiglitazone-induced improvements of insulin sensitivity result from two convergent mechanisms: increased insulin receptor expression and insulin receptor activation.
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