Glucose starvation and glycosylation inhibitors reduce insulin receptor gene expression: characterization and potential mechanism in human cells

Biochem Biophys Res Commun. 1990 Jun 15;169(2):397-405. doi: 10.1016/0006-291x(90)90345-n.

Abstract

Glucose affects the expression of several genes in many cell types. In this work (i) we stably cultured three human cell lines in media containing different glucose concentrations (from 0 to 25 mM), (ii) we characterized glucose effects on insulin receptor gene expression, (iii) we investigated the mechanism by which glucose produces these effects. We found that: (i) glucose starvation reduces insulin receptor gene expression likely affecting insulin receptor gene transcription rates; (ii) a hexose that undergoes to interconversion with glucose metabolites (D-fructose), added to low-glucose media, increases either insulin receptor mRNA levels or insulin binding activity, while hexoses unable to enter the cell (L-glucose) or not metabolizable (3-O-methylglucose), do not produce any effect; (iii) glycosylation inhibitors (2-deoxyglucose and tunicamycin) reduce, in a time-dependent manner, insulin receptor mRNA levels. Our data indicate that glucose affects insulin receptor gene expression in human cells and that protein glycosylation plays a role in this regulatory mechanism.

MeSH terms

  • Blotting, Northern
  • Cell Line
  • Gene Expression Regulation* / drug effects
  • Glucose / pharmacology*
  • Hexoses / pharmacology
  • Humans
  • Insulin / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Kinetics
  • RNA / genetics
  • RNA / isolation & purification
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / isolation & purification
  • Receptor, Insulin / biosynthesis
  • Receptor, Insulin / genetics*
  • Receptor, Insulin / metabolism
  • Receptors, Cell Surface / metabolism
  • Receptors, Somatomedin
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / metabolism

Substances

  • Hexoses
  • Insulin
  • RNA, Neoplasm
  • Receptors, Cell Surface
  • Receptors, Somatomedin
  • RNA
  • Insulin-Like Growth Factor I
  • Receptor, Insulin
  • Glucose