Evidence that metformin increases insulin-stimulated glucose transport by potentiating insulin-induced translocation of glucose transporters from an intracellular pool to the cell surface in rat adipocytes

Horm Metab Res Suppl. 1992:26:34-41.

Abstract

To examine the cellular mechanism of the antihyperglycemic action of metformin (M) we studied the effect of M on various functional and molecular parameters involved in the pathogenesis of insulin resistance. Isolated rat adipocytes were incubated with or without M (1-100 micrograms/ml) for 2 hours at 37 degrees C followed by an incubation with or without insulin (I) (10) ng/ml). M-treatment had no significant effect on basal (B) 3-O-methylglucose uptake. In contrast, M increased I-stimulated glucose transport in a dose dependent manner up to 43 +/- 7%. This effect was neither associated with a significant effect of M on trace insulin binding, 1.74 +/- .2% (-M) vs 1.89 +/- .3% (+M), p > 0.05, nor with an effect of M on in vivo activation of insulin receptor kinase activity as measured by 32P-incorporation into the 95 kDa beta-subunit of the insulin receptor and an exogenous substrate, histone 2B.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

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

MeSH terms

  • Adipose Tissue / cytology
  • Adipose Tissue / drug effects*
  • Adipose Tissue / metabolism
  • Animals
  • Biological Transport / drug effects
  • Blood Glucose / metabolism*
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Gene Expression Regulation / physiology
  • Insulin / metabolism
  • Insulin / physiology*
  • Male
  • Metformin / pharmacology*
  • Monosaccharide Transport Proteins / genetics
  • Monosaccharide Transport Proteins / physiology*
  • Protein-Tyrosine Kinases / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, Insulin

Substances

  • Blood Glucose
  • Insulin
  • Monosaccharide Transport Proteins
  • Metformin
  • Protein-Tyrosine Kinases
  • Receptor, Insulin