GLUCOCORTICOID HORMONE-BINDING TO RAT ADIPOCYTES

Previous quantification of glucocorticoid receptor (GR) binding in adipose tissue has been performed in cytosol preparations, which did not allow the determination of the total number of GR in the cell. Therefore, GR binding was determined in intact adipocytes. Dexamethasone (dex) was used as a ligand in adipocytes isolated from epididymal (Epi), retroperitoneal (Ret), inguinal (Ing) and mesenteric (Mes) adipose tissue regions in male rats. The binding was saturable and specific with a K-d in the nanomolar range, not different from previously reported affinity of binding in cytosol preparations from adipocytes. Binding capacity rose after removal of endogenous glucocorticoids either by adrenalectomy (ADX) or culture in a glucocorticoid-free medium. Binding capacity of adipocytes was in general higher in Mes adipose cells than in adipocytes from Epi, Ing and Ret tissues from intact and ADX animals when expressed per unit of triglyceride weight of adipose tissues. This seemed to be largely explainable by a higher cellular density in Mes than in other adipose tissues. When comparisons were performed with binding per adipocyte, intraabdominal (Epi, Ret and Mes) cells bound more dex than adipocytes from subcutaneous (Ing) adipose tissue. It is suggested that in comparison with other adipose tissues Mes tissue has a higher density of the GR in situ, due mainly to a higher cellular density. Intraabdominal adipocytes in general seem to have a higher GR density than subcutaneous cells. This might explain the high activity of glucocorticoid-regulated metabolic pathways in intraabdominal, particularly Mes adipose tissue.