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

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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.

Original languageEnglish
Pages (from-to)397-405
Number of pages9
JournalBiochemical and Biophysical Research Communications
Volume169
Issue number2
DOIs
Publication statusPublished - Jun 15 1990

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Glycosylation
Insulin Receptor
Starvation
Gene expression
Cells
Gene Expression
Glucose
Hexoses
Genes
3-O-Methylglucose
Tunicamycin
Messenger RNA
Deoxyglucose
Transcription
Metabolites
Fructose
Insulin
Cell Line

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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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.",
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