TNFα release by the nonfat cells of human adipose tissue

• Published in: International Journal of Obesity 2004-04, Vol.28 (4), p.616-622
• Main Authors: Fain, J N, Bahouth, S W, Madan, A K
• Format: Article
• Language: English
• Subjects: Adipose tissues; Biological and medical sciences; Epidemiology; Genetic aspects; Health aspects; Health Promotion and Disease Prevention; Internal Medicine; Medical sciences; Medicine; Medicine & Public Health; Metabolic Diseases; Obesity; Overweight persons; Public Health; Tumor necrosis factor
• ISSN: 0307-0565; 1476-5497
• DOI: 10.1038/sj.ijo.0802594

OBJECTIVE: The primary aim was to investigate the relative importance of the adipocytes vs the nonfat cells present in human adipose tissue with respect to release of immunoreactive tumor necrosis factor- α (TNF α ). The second aim was to examine the correlation between body mass index (BMI) and the subsequent release of adiponectin and TNF α by explants of human subcutaneous and visceral adipose tissue incubated in primary culture for 48 h. RESULTS: We found that the maximal release of TNF α was seen during the first 4 h of a 48-h incubation by explants of human adipose tissue in primary culture. Over 95% of the TNF α released to the medium by human adipose tissue explants over a 4-h incubation came from the nonfat cells present in the adipose tissue. The release of TNF α by the nonfat cells released during collagenase digestion was slightly higher than that by the cells present in the adipose tissue matrix after collagenase digestion. TNF α release by the combined matrix and isolated nonfat cells was greater than that by explants of tissue indicating some upregulation induced by collagenase digestion. Immunoreactive TNF α disappeared from the medium with a half-time of approximately 10 h. There was a positive correlation coefficient of 0.79 between TNF α release by tissue explants and the BMI of the fat donors as well as a correlation of 0.52 between BMI and release by adipocytes. TNF α release negatively correlated [−0.60] with adiponectin release by adipose tissue. The release of TNF α was far less than that of adiponectin or IL-6, and less than that of plasminogen activator inhibitor-1, hepatocyte growth factor, or leptin over a 4-h incubation of human adipose tissue explants. TNF α release over 4 h was enhanced by lipopolysaccharide and inhibited by a cyclooxygenase-2 inhibitor. CONCLUSION: The release of TNF α by adipose tissue of obese humans is primarily due to the nonfat cells present in adipose tissue. TNF α is a short-lived adipokine whose release by human adipose tissue in primary culture correlates with the BMI of the fat donors.