Adipose tissue is a major source of inflammatory and thrombotic cytokines. This study investigated the relationship of abdominal subcutaneous adipose tissue cytokine gene expression to body composition, fat distribution, and metabolic risk during obesity. We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-α, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 ± 0.8 kg/m2; age, 57 ± 1 yr). A subset of these women without diabetes ( n = 15) also underwent an OGTT. In all women, visceral fat volume was negatively related to leptin ( r = −0.46, P < 0.05) and tended to be negatively related to adiponectin ( r = −0.38, P = 0.09) gene expression. Among the nondiabetic women, fasting insulin ( r = 0.69, P < 0.01), 2-h insulin ( r = 0.56, P < 0.05), and HOMA index ( r = 0.59, P < 0.05) correlated positively with TNF-α gene expression; fasting insulin ( r = 0.54, P < 0.05) was positively related to, and 2-h insulin ( r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area ( r = −0.56, P < 0.05) was negatively related to, and insulin area ( r = −0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression. Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-β-actin ratio, 2.26 ± 0.46 vs. 3.31 ± 0.33, P < 0.05). We conclude that abdominal subcutaneous adipose tissue expression of inflammatory cytokines is a potential mechanism linking obesity with its metabolic comorbidities.
885 The secretion of TNF-α by inflammatory macrophages has dual effects on subcutaneous adipose precursor cells: inhibition of differentiation and activation of proliferation
