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Diabetes 53:41-52, 2004
© 2004 by the American Diabetes Association, Inc.

Dehydroepiandrosterone Stimulates Glucose Uptake in Human and Murine Adipocytes by Inducing GLUT1 and GLUT4 Translocation to the Plasma Membrane

Sebastio Perrini1, Annalisa Natalicchio1, Luigi Laviola1, Gaetana Belsanti1, Carmela Montrone1, Angelo Cignarelli1, Vincenza Minielli2, Maria Grano2, Giovanni De Pergola1, Riccardo Giorgino1, and Francesco Giorgino1

1 Department of Emergency and Organ Transplantation, Section on Internal Medicine, Endocrinology and Metabolic Diseases, Bari, Italy
2 Department of Human Anatomy and Histology, University of Bari, Bari, Italy

Dehydroepiandrosterone (DHEA) has been shown to modulate glucose utilization in humans and animals, but the mechanisms of DHEA action have not been clarified. We show that DHEA induces a dose- and time-dependent increase in glucose transport rates in both 3T3-L1 and human adipocytes with maximal effects at 2 h. Exposure of adipocytes to DHEA does not result in changes of total GLUT4 and GLUT1 protein levels. However, it does result in significant increases of these glucose transporters in the plasma membrane. In 3T3-L1 adipocytes, DHEA increases tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 and stimulates IRS-1- and IRS-2-associated phosphatidylinositol (PI) 3-kinase activity with no effects on either insulin receptor or Akt phosphorylation. In addition, DHEA causes significant increases of cytosolic Ca2+ concentrations and a parallel activation of protein kinase C (PKC)-ß2. The effects of DHEA are abrogated by pretreatment of adipocytes with PI 3-kinase and phospholipase C{gamma} inhibitors, as well as by inhibitors of Ca2+-dependent PKC isoforms, including a specific PKC-ß inhibitor. Thus, DHEA increases glucose uptake in both human and 3T3-L1 adipocytes by stimulating GLUT4 and GLUT1 translocation to the plasma membrane. PI 3-kinase, phospholipase C{gamma}, and the conventional PKC-ß2 seem to be involved in DHEA effects.

Address correspondence and reprint requests to Francesco Giorgino, MD, PhD, Department of Emergency and Organ Transplantation, Section on Internal Medicine, Endocrinology and Metabolic Diseases, University of Bari, Piazza Giulio Cesare, 11, I-70124 Bari, Italy. E-mail: f.giorgino{at}endo.uniba.it


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Copyright © 2004 by the American Diabetes Association.