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Related Experiment Videos

Muscle uridine diphosphate-hexosamines do not decrease despite correction of hyperglycemia-induced insulin resistance

Marie-Jose J Pouwels1, Paul N Span, Cees J Tack

  • 1Division of General Internal Medicine, Department of Medicine, University Medical Center, 6500 HB Nijmegen, The Netherlands. m.j.pouwels@club.tip.nl

The Journal of Clinical Endocrinology and Metabolism
|November 5, 2002
PubMed
Summary

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High blood sugar causes insulin resistance in type 2 diabetes. This study found that correcting high blood sugar in patients increased, not decreased, key hexosamine pathway products in muscle, challenging a common hypothesis.

Area of Science:

  • Metabolic disorders
  • Endocrinology
  • Biochemistry

Background:

  • Hyperglycemia is linked to insulin resistance in type 2 diabetes mellitus (DM).
  • Animal studies suggest the hexosamine pathway, producing UDP-N-acetylglucosamine (UDP-GlcNAc) and UDP-N-acetylgalactosamine (UDP-GalNAc), is implicated in this process.

Purpose of the Study:

  • To investigate the role of the hexosamine pathway in hyperglycemia-induced insulin resistance in human patients with type 2 DM.
  • To measure changes in UDP-hexosamine levels in skeletal muscle following euglycemia.

Main Methods:

  • Eight obese patients with uncontrolled type 2 DM and severe insulin resistance were treated with intravenous insulin to achieve euglycemia.
  • Insulin sensitivity was assessed using hyperinsulinemic euglycemic clamp before and after treatment.

Related Experiment Videos

  • Muscle biopsies were analyzed for UDP-GlcNAc, UDP-GalNAc, UDP-glucose, and UDP-galactose levels.

    • Main Results:

    • Euglycemia significantly improved insulin resistance, evidenced by increased glucose infusion rates and decreased insulin requirements.
    • Contrary to the hypothesis, UDP-GlcNAc and UDP-GalNAc concentrations in skeletal muscle significantly increased after achieving euglycemia.
    • Serum transferrin isoelectric focusing patterns and urinary glycosaminoglycan excretion remained unchanged.

    Conclusions:

    • The study's findings do not support the hypothesis that increased UDP-hexosamine accumulation is a primary mechanism driving hyperglycemia-induced insulin resistance in type 2 DM patients.
    • Elevated UDP-hexosamine levels in skeletal muscle may be a consequence rather than a cause of improved insulin sensitivity in this context.