Human GLUT-2 overexpression does not affect glucose-stimulated insulin secretion in MIN6 cells

Am J Physiol. 1995 Nov;269(5 Pt 1):E897-902. doi: 10.1152/ajpendo.1995.269.5.E897.

Abstract

Accumulated evidence suggests that GLUT-2, in addition to its role in glucose transport, may also have other functions in glucose-stimulated insulin secretion. As a first step in addressing this possibility, we have engineered MIN6 cells overexpressing human GLUT-2 by transfection with human GLUT-2 cDNA. Stable transformants harboring human GLUT-2 cDNA exhibited an approximately twofold increase in 3-O-methyl-D-glucose uptake at 0.5 and 15 mM. Glucokinase activity or glucose utilization measured by conversion of [5-3H]glucose to [3H]H2O was not, however, altered in the MIN6 cells overexpressing human GLUT-2. Furthermore, glucose-stimulated insulin secretion was not affected by over-expression of human GLUT-2. An abundance of GLUT-2, therefore, does not correlate with the glucose responsiveness of cells in which glycolysis is regulated at the glucose phosphorylating step. These data suggest that GLUT-2 by itself does not have significant functions other than its role in glucose transport in glucose sensing by MIN6 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-O-Methylglucose
  • Cell Line
  • Glucose / metabolism
  • Glucose / pharmacology*
  • Glucose Transporter Type 2
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / metabolism*
  • Methylglucosides / pharmacokinetics
  • Monosaccharide Transport Proteins / metabolism*
  • Phosphorylation
  • Subcellular Fractions / metabolism
  • Tissue Distribution
  • Transfection

Substances

  • Glucose Transporter Type 2
  • Insulin
  • Methylglucosides
  • Monosaccharide Transport Proteins
  • 3-O-Methylglucose
  • Glucose