Dexamethasone causes translocation of glucose transporters from the plasma membrane to an intracellular site in human fibroblasts.

摘要: Abstract To investigate the mechanism by which glucocorticoids inhibit glucose transport in peripheral tissues, we have used a monoclonal antibody directed against human transporter to measure relative amounts of polypeptide various cell fractions foreskin fibroblasts after treatment with and without dexamethasone. In cells treated for 4 h 100 nM dexamethasone, decrease 48% was accompanied 40% amount plasma membrane fraction enriched 10-fold 5'-nucleotidase activity 78% increase putative intracellular membranes, designated P2. There no significant change whole lysates. Insulin (200 nM) stimulated basal only 9%. However, addition insulin 30 min that had been dexamethasone completely reversed dexamethasone-induced also changes content P2 fractions. From these observations conclude decreases causing translocation transporters from an internal location reverses effect reversing translocation.