High glucose and insulin promote O-GlcNAc modification of proteins, including alpha-tubulin

Am J Physiol Endocrinol Metab. 2003 Feb;284(2):E424-34. doi: 10.1152/ajpendo.00382.2002. Epub 2002 Oct 22.

Abstract

Increased flux through the hexosamine biosynthesis pathway has been implicated in the development of glucose-induced insulin resistance and may promote the modification of certain proteins with O-linked N-acetylglucosamine (O-GlcNAc). L6 myotubes (a model of skeletal muscle) were incubated for 18 h in 5 or 25 mM glucose with or without 10 nM insulin. As assessed by immunoblotting with an O-GlcNAc-specific antibody, high glucose and/or insulin enhanced O-GlcNAcylation of numerous proteins, including the transcription factor Sp1, a known substrate for this modification. To identify novel proteins that may be O-GlcNAc modified in a glucose concentration/insulin-responsive manner, total cell membranes were separated by one- or two-dimensional gel electrophoresis. Selected O-GlcNAcylated proteins were identified by mass spectrometry (MS) analysis. MS sequencing of tryptic peptides identified member(s) of the heat shock protein 70 (HSP70) family and rat alpha-tubulin. Immunoprecipitation/immunoblot studies demonstrated several HSP70 isoforms and/or posttranslational modifications, some with selectively enhanced O-GlcNAcylation following exposure to high glucose plus insulin. In conclusion, in L6 myotubes, Sp1, membrane-associated HSP70, and alpha-tubulin are O-GlcNAcylated; the modification is markedly enhanced by sustained increased glucose flux.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylglucosamine / metabolism
  • Animals
  • Cells, Cultured
  • Glucose / pharmacology*
  • Glycosylation / drug effects
  • HSP70 Heat-Shock Proteins / metabolism
  • Hypoglycemic Agents / pharmacology*
  • Insulin / pharmacology*
  • Insulin Resistance / physiology
  • Mass Spectrometry
  • Membrane Proteins / metabolism
  • Muscle Cells / cytology
  • Muscle Cells / metabolism*
  • Sp1 Transcription Factor / metabolism
  • Tubulin / metabolism*

Substances

  • HSP70 Heat-Shock Proteins
  • Hypoglycemic Agents
  • Insulin
  • Membrane Proteins
  • Sp1 Transcription Factor
  • Tubulin
  • Glucose
  • Acetylglucosamine