Oxidative stress-induced insulin resistance in skeletal muscle cells is ameliorated by gamma-tocopherol treatment.

Abstract

BACKGROUND:

Oxidative stress-induced reactive oxygen species are associated with the clinical manifestation of insulin resistance. Evidence suggests that antioxidant treatment may reduce this incidence.

AIM OF THE STUDY:

This study determined whether glucose oxidase (GO)-induced insulin resistance in cultured skeletal muscle cells could be ameliorated by pre-treatment with gamma-tocopherol (GT).

METHODS:

Insulin sensitivity in L6 myotubes was assessed by 2-deoxy-D: -[(3)H]-glucose uptake. The phosphorylation of distal insulin signaling proteins Akt and the Akt substrate AS160 were determined by western blot.

RESULTS:

One hour treatment with 100 mU/ml GO decreased insulin-stimulated glucose uptake (P < 0.001). Pre-treatment with GT either partially (100 microM) or completely (200 microM) restored insulin-stimulated glucose uptake in cells after GO-induced insulin resistance. GO-induced oxidative stress did not impair insulin stimulated phosphorylation of Akt or AS160, but 200 microM GT increased insulin-stimulated phosphorylation of these key signaling proteins (P < 0.05).

CONCLUSIONS:

High-dose (200 microM) GT treatment ameliorated oxidative stress-induced insulin resistance in cultured rat L6 skeletal muscle cells.

• Authors: Indu Singh, Andrew L Carey, Nadine Watson, Mark A Febbraio, John A Hawley
• Journal: European journal of nutrition (Eur J Nutr) Vol. 47 Issue 7 Pg. 387-92 (Oct 2008) ISSN: 1436-6215 [Electronic] Germany
• PMID: 18807106 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Blood Glucose
• Insulin
• Reactive Oxygen Species
• gamma-Tocopherol
• Glucose Oxidase
• Proto-Oncogene Proteins c-akt

Topics

• Analysis of Variance
• Animals
• Blood Glucose (metabolism)
• Blotting, Western
• Cells, Cultured
• Glucose Oxidase (toxicity)
• Humans
• Insulin (metabolism)
• Insulin Resistance
• Muscle, Skeletal (metabolism, physiology)
• Oxidative Stress (drug effects)
• Phosphorylation
• Proto-Oncogene Proteins c-akt (metabolism)
• Rats
• Reactive Oxygen Species
• gamma-Tocopherol (pharmacology)