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Diabetes Obes Metab. 2004 Jul;6(4):293-8.

Glucosamine-induced insulin resistance in L6 muscle cells.

Author information

1
School of Life and Health Sciences, Aston University, Birmingham, UK. c.j.bailey@aston.ac.uk

Abstract

BACKGROUND:

Glucosamine increases flux through the hexosamine pathway, causing insulin resistance and disturbances similar to diabetic glucose toxicity.

AIM:

This study examines the effect of glucosamine on glucose uptake by cultured L6 muscle cells as a model of insulin resistance.

METHODS:

Glucose uptake by L6 myotubes was measured using the non-metabolized glucose analogue 2-deoxy-d-glucose after incubation with glucosamine for 4 and 24 h, with and without insulin and several other agents (metformin, peroxovanadium and d-pinitol) that improve glucose uptake in diabetic states.

RESULTS:

After 4 h, high concentrations of glucosamine (5 x 10(-3) and 10(-2) M) reduced basal and insulin-stimulated glucose uptake by up to 50%. After 24 h, the effect of insulin was completely abolished by 10(-2) M glucosamine and reduced over 50% by 5 x 10(-3) M glucosamine. Lower concentrations of glucosamine did not significantly alter glucose uptake. The effect of glucosamine could not be attributed to cytotoxicity assessed by the Trypan Blue test. Metformin, peroxovanadium and d-pinitol, each of which increased glucose uptake by L6 cells, did not prevent the decrease in glucose uptake with glucosamine.

CONCLUSION:

Glucosamine decreased insulin-stimulated glucose uptake by L6 muscle cells, providing a potential model of insulin resistance with similarities to glucose toxicity. Insulin resistance induced by glucosamine was not reversed by three agents (metformin, peroxovanadium and d-pinitol) known to enhance or partially mimic the effects of insulin.

[Indexed for MEDLINE]

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