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Tumor Necrosis Factor- Inhibits Leptin Production in Subcutaneous and Omental Adipocytes from Morbidly Obese Humans¹

Division of Endocrinology and Metabolism, Departments of Medicine (L.B.W., R.L.F., A.S.W., Z.P., R.L., R.V.C.) and Surgery (R.M.J.), Indiana University School of Medicine, Indianapolis, Indiana 46202; and the Department of Surgery, St. Vincent’s Hospital Carmel (R.M.J., M.I., J.H.), Carmel, Indiana 46032

Address all correspondence and requests for reprints to: Robert V. Considine, Ph.D., Indiana University School of Medicine, 541 North Clinical Drive, Clinical Building 455, Indianapolis, Indiana 46202-5111. E-mail: rconsidi{at}iupui.edu

This study was undertaken to examine the regulation of leptin production from human adipocytes by tumor necrosis factor- (TNF). Adipocytes were isolated from adipose tissue obtained during bariatric surgical procedures (17 women and 3 men; body mass index, 52.5 ± 2.4 kg/m²; age, 40 ± 3 yr) and cultured in suspension. Leptin release from SC adipocytes was inhibited 17.7 ± 5.2% (P < 0.01), 21.6 ± 4.3% (P < 0.005), and 37.1 ± 7.2% (P < 0.05) by 1, 10, and 100 ng/mL TNF, respectively, after 48 h in culture. At 100 ng/mL, significant inhibition of leptin release (25.8 ± 9.7%; P < 0.05) was detected by 24 h. TNF (10 ng/mL) had no effect on dexamethasone (0.1 µmol/L)-stimulated leptin production in sc adipocytes. In omental adipocytes TNF inhibited leptin release 21.0 ± 9.6% and 40.8 ± 6.3% at 10 and 100 ng/mL by 48 h (P < 0.05). Significant inhibition of leptin release from omental adipocytes was observed at 24 h with 100 ng/mL TNF (P < 0.05). Anti-TNF antibody completely blocked TNF inhibition of leptin release. The ob messenger ribonucleic acid was significantly reduced (23.6 ± 5.9%) after 48 h of TNF (100 ng/mL) treatment (P < 0.025). TNF had no effect on glucose uptake or lactate production in SC and omental adipocytes. The data suggest that the direct paracrine effect of adipose-derived TNF is inhibition of leptin production.

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