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The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 12 5662-5667
Copyright © 2002 by The Endocrine Society


Original Article

Differential Regulation of Adiponectin Secretion from Cultured Human Omental and Subcutaneous Adipocytes: Effects of Insulin and Rosiglitazone

Hiroyuki Motoshima, Xiangdong Wu, Madhur K. Sinha, V. Elise Hardy, Ernest L. Rosato, Donna J. Barbot, Francis E. Rosato and Barry J. Goldstein

Dorrance H. Hamilton Research Laboratories, Division of Endocrinology, Diabetes, and Metabolic Diseases, Department of Medicine (H.M., X.W., V.E.H., B.J.G.), and Department of Surgery (E.L.R., D.J.B., F.E.R.), Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107; and Linco Research, Inc. (M.K.S.), St. Charles, Missouri 63304

Address all correspondence and requests for reprints to: Barry J. Goldstein, M.D., Ph.D., Director, Division of Endocrinology and Metabolic Diseases, Jefferson Medical College, Room 349 Alumni Hall, 1020 Locust Street, Philadelphia, Pennsylvania 19107-6799. E-mail: barry.goldstein{at}mail.tju.edu.

Abstract

Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and antiatherosclerotic properties. Because adipose tissue depots differ in the strength of their association with the adverse metabolic consequences of obesity, we studied the secretion of adiponectin in vitro from paired samples of isolated human omental and sc adipocytes and its regulation by insulin and rosiglitazone. Cells were incubated for 12 or 24 h with and without treatment with 100 nM insulin, 8 µM rosiglitazone, or both combined; adiponectin secreted into the culture medium was measured by a RIA with a human adiponectin standard and normalized for cellular DNA content. Secretion of adiponectin by omental cells was generally higher than sc cells and showed a strong negative correlation with body mass index (r = -0.78;P = 0.013). In contrast, secretion from the sc cells was unrelated to body mass index. Compared with sc-derived adipocytes, adiponectin secretion from omental cells was increased by insulin or rosiglitazone alone and was up to 2.3-fold higher following combined treatment with insulin and rosiglitazone, whereas secretion from sc adipose cells was unaffected by these treatments. These data suggest that reduced secretion from the omental adipose depot may account for the decline in plasma adiponectin observed in obesity. Furthermore, enhanced adiponectin secretion from fat cells derived from the visceral compartment in response to rosiglitazone alone or in combination with insulin may play a role in some of the systemic insulin-sensitizing and antiinflammatory properties of the thiazolidinediones.




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