Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.

@article{Cooksey1999MechanismOH,
  title={Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.},
  author={Robert C. Cooksey and L F Hebert and Jun Hui Zhu and Perisco Wofford and W Timothy Garvey and Donald A. McClain},
  journal={Endocrinology},
  year={1999},
  volume={140 3},
  pages={1151-7}
}
Hexosamines have been hypothesized to mediate aspects of glucose sensing and toxic effects of hyperglycemia. For example, insulin resistance results when the rate-limiting enzyme for hexosamine synthesis, glutamine:fructose-6-phosphate amidotransferase (GFA), is overexpressed in muscle and adipose tissue of transgenic mice. The glucose infusion rates required to maintain euglycemia at insulin infusion rates of 0.5, 2, 15, and 20 mU/kg x min were 39-90% lower in such transgenic mice, compared… CONTINUE READING

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Glucosamineinduced inhibition of liver glucokinase impairs the ability of hyperglycemia to suppress endogenous glucose production

N Barzilai, M Hawkins, I Angelox, M Hu, L Rossetti
Diabetes • 1996
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