The phorbol ester TPA induces a translocation of the insulin sensitive glucose carrier (GLUT4) in fat cells

Biochem Biophys Res Commun. 1990 May 16;168(3):1089-94. doi: 10.1016/0006-291x(90)91141-e.

Abstract

Insulin activates the glucose transport in isolated fat cells through a translocation of the insulin sensitive glucose carrier subtype (GLUT4) and by activation of glucose carriers in the plasma membrane. Protein kinase C stimulating phorbol esters are able to mimick partially the insulin effect on glucose transport. In order to determine whether this phorbol ester effect occurs through a translocation of the insulin sensitive glucose carrier (GLUT4) we used a monoclonal antibody against GLUT4 to determine its distribution in subcellular fractions of rat adipocytes. We found that the phorbol ester TPA is able to increase the amount of GLUT4 in the plasma membrane fraction about two-fold.

MeSH terms

  • Adipose Tissue / cytology
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Animals
  • Antibodies, Monoclonal
  • Blotting, Western
  • Cytochalasin B / metabolism
  • Glucose / metabolism*
  • Insulin / physiology
  • Male
  • Monosaccharide Transport Proteins / metabolism*
  • Protein Kinase C / physiology
  • Rats
  • Rats, Inbred Strains
  • Subcellular Fractions
  • Tetradecanoylphorbol Acetate / pharmacology*

Substances

  • Antibodies, Monoclonal
  • Insulin
  • Monosaccharide Transport Proteins
  • Cytochalasin B
  • Protein Kinase C
  • Glucose
  • Tetradecanoylphorbol Acetate