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Cited by 405Biochemical Acid Research StudiesMetabolism, Diabetes, and CancerNatural Antidiabetic Agents Studies

Protection Against Oxidative Stress—Induced Insulin Resistance in Rat L6 Muscle Cells by Micromolar Concentrations of α-Lipoic Acid

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Maddux, Betty A., See, Wendy, Lawrence, John C., Goldfine, Amy L., Goldfine, Ira D., Evans, Joseph L.·2001·Diabetes
DOI 10.2337/diabetes.50.2.404
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Abstract

In diabetic patients, α-lipoic acid (LA) improves skeletal muscle glucose transport, resulting in increased glucose disposal; however, the molecular mechanism of action of LA is presently unknown. We studied the effects of LA on basal and insulin-stimulated glucose transport in cultured rat L6 muscle cells that overexpress GLUT4. When 2-deoxy-D-glucose uptake was measured in these cells, they were more sensitive and responsive to insulin than wild-type L6 cells. LA, at concentrations ≤1 mmol/l, had only small effects on glucose transport in cells not exposed to oxidative stress. When cells were exposed to glucose oxidase and glucose to generate H2O2 and cause oxidative stress, there was a marked decrease in insulin-stimulated glucose transport. Pretreatment with LA over the concentration range of 10-1,000 μmol/l protected the insulin effect from inhibition by H2O2. Both the R and S isomers of LA were equally effective. In addition, oxidative stress caused a significant decrease (∼50%) in reduced glutathione concentration, along with the rapid activation of the stress-sensitive p38 mitogen-activated protein kinase. Pretreatment with LA prevented both of these events, coincident with protecting insulin action. These studies indicate that in muscle, the major site of insulin-stimulated glucose disposal, one important effect of LA on the insulin-signaling cascade is to protect cells from oxidative stress-induced insulin resistance.

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Authors
Maddux, B. A., See, W., Lawrence, J. C., Goldfine, A. L., Goldfine, I. D., & Evans, J. L.
Affiliations
University of Virginia (US)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2001-02-01
Volume
50
Issue
2
Pages
404-410
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.50.2.404
OpenAlex
W2100066777
Cited by
405
References
54
Citations by year
2026: 1 · 2025: 6 · 2024: 18 · 2023: 11 · 2022: 11 · 2021: 15 · 2020: 14 · 2019: 13 · 2018: 12 · 2017: 10 · 2016: 14 · 2015: 23 · 2014: 21 · 2013: 30 · 2012: 21
FWCI
4.27
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
American Diabetes Association
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Biochemical Acid Research Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Keywords
alpha-lipoic acid, insulin resistance, oxidative stress, insulin-stimulated glucose transport, skeletal muscle, GLUT4, hydrogen peroxide, p38 MAPK, glutathione, L6 cells
MeSH terms
Animals, Cell Line, Enzyme Activation, Glucose, Glucose Oxidase, Glutathione, Hydrogen Peroxide, Insulin, Insulin Resistance, Intracellular Membranes, L-Lactate Dehydrogenase, Thioctic Acid, Monosaccharide Transport Proteins, Muscle Proteins, Osmolar Concentration, Reference Values, Oxidants, Cell Death, Oxidative Stress, Muscle, Skeletal, Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Glucose Transporter Type 4, Rats

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