Tumor necrosis factor-α inhibits leptin production in subcutaneous and omental adipocytes from morbidly obese humans

Rachael L. Fawcett, Angela S. Waechter, Lloyd B. Williams, Peili Zhang, Raymond Louie, Rosemarie Jones, Margaret Inman, John Huse, Robert V. Considine

Research output: Contribution to journalArticle

55 Scopus citations

Abstract

This study was undertaken to examine the regulation of leptin production from human adipocytes by tumor necrosis factor-α (TNFα). 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 TNFα, 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. TNFα (10 ng/mL) had no effect on dexamethasone (0.1 μmol/L)-stimulated leptin production in sc adipocytes. In omental adipocytes TNFα 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 TNFα (P < 0.05). Anti-TNFα antibody completely blocked TNFα inhibition of leptin release. The ob messenger ribonucleic acid was significantly reduced (23.6 ± 5.9%) after 48 h of TNFα (100 ng/mL) treatment (P < 0.025). TNFα 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 TNFα is inhibition of leptin production.

Original languageEnglish (US)
Pages (from-to)530-535
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume85
Issue number2
DOIs
StatePublished - 2000

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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