Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance

American Journal of Physiology - Endocrinology and Metabolism - Tập 280 Số 5 - Trang E745-E751 - 2001
Philip A. Kern1, Subramanian Ranganathan1, Chunling Li1, Linda C. Wood1, Gouri Ranganathan1
1Division of Endocrinology, Department of Medicine, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205

Tóm tắt

Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. We measured TNF and IL-6 expression in the adipose tissue of 50 lean and obese subjects without diabetes. Insulin sensitivity (SI) was determined by an intravenous glucose tolerance test with minimal-model analysis. When lean [body mass index (BMI) <25 kg/m2] and obese (BMI 30–40 kg/m2) subjects were compared, there was a 7.5-fold increase in TNF secretion ( P < 0.05) from adipose tissue, and the TNF secretion was inversely related to SI( r = −0.42, P < 0.02). IL-6 was abundantly expressed by adipose tissue. In contrast to TNF, plasma (rather than adipose) IL-6 demonstrated the strongest relationship with obesity and insulin resistance. Plasma IL-6 was significantly higher in obese subjects and demonstrated a highly significant inverse relationship with SI ( r = −0.71, P < 0.001). To separate the effects of BMI from SI, subjects who were discordant for SI were matched for BMI, age, and gender. By use of this approach, subjects with low SI demonstrated a 3.0-fold increased level of TNF secretion from adipose tissue and a 2.3-fold higher plasma IL-6 level ( P < 0.05) compared with matched subjects with a high SI. Plasma IL-6 was significantly associated with plasma nonesterified fatty acid levels ( r = 0.49, P < 0.002). Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance.

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Tài liệu tham khảo

Arner P., 1996, Diabet Med, 13, S85, 10.1002/dme.1996.13.s6.85

Bastard JP, 2000, J Clin Endocrinol Metab, 85, 3338

10.1016/1043-4666(94)90067-1

10.1210/edrv-6-1-45

10.1172/JCI110398

10.1172/JCI112886

10.2337/diab.46.1.3

10.1093/oxfordjournals.aje.a009158

10.1210/endo.139.12.6336

10.1038/sj.ijo.0800826

10.1016/0303-7207(96)03761-6

Dandona P, 1998, J Clin Endocrinol Metab, 83, 2907

10.1210/endo.130.1.1370149

10.1016/0092-8674(95)90445-X

Fried SK, 1998, J Clin Endocrinol Metab, 83, 847

Greenberg AS, 1992, Cancer Res, 52, 4113

10.1172/JCI117936

10.1172/JCI117495

10.1126/science.274.5291.1377

10.1126/science.7678183

10.2337/diab.43.11.1271

10.2337/diab.42.11.1663

10.1093/jn/127.9.1917S

10.1172/JCI117899

10.1001/jama.1994.03520030047027

10.2337/diabetes.49.5.688

10.2337/diab.44.9.1121

10.1126/science.1439783

Mohamed-Ali V, 1997, J Clin Endocrinol Metab, 82, 4196

10.1001/jama.282.16.1519

10.2337/diab.45.7.881

Orban Z, 1999, J Clin Endocrinol Metab, 84, 2126

Paquot N, 2000, J Clin Endocrinol Metab, 85, 1316

10.1073/pnas.83.21.8313

10.1055/s-2007-979001

10.1046/j.1525-1373.2000.22318.x

10.1172/JCI2849

10.1152/jappl.1985.58.5.1565

10.2337/diab.44.8.863

10.1038/39335

10.1210/jcem-71-6-1508

10.1046/j.1464-5491.1999.00052.x

Zinman B, 1999, J Clin Endocrinol Metab, 84, 272

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American Journal of Physiology - Endocrinology and Metabolism

Tập 280 Số 5

E745-E751

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