TNFα expression of subcutaneous adipose tissue in obese and morbid obese females:: relationship to adipocyte LPL activity and leptin synthesis

被引:76
作者
Bulló, M
García-Lorda, P
Peinado-Onsurbe, J
Hernández, M
Del Castillo, D
Argilés, JM
Salas-Salvadó, J
机构
[1] Univ Rovira & Virgili, Unitat Nutr Humana, Fac Med & Ciencies Salut Reus, E-43201 Reus, Spain
[2] Univ Barcelona, Fac Biol, Unitat Bioquim & Biol Mol, E-08007 Barcelona, Spain
[3] Hosp Univ St Joan, Serv Cirurg, Reus, Spain
[4] Hosp Univ St Joan, Med Interna Serv, Reus, Spain
关键词
leptin; TNF alpha; sTNFR; LPL activity; obesity; diabetes mellitus;
D O I
10.1038/sj.ijo.0801977
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
INTRODUCTION: Tumor necrosis factor (TNFalpha) has been invoked as an adipostat. Accordingly, the adipose tissue expression of TNFalpha has been shown to be proportional to the degree of adiposity. The regulatory role of TNFalpha in obesity may be controlled by several mechanisms. These include the inhibitory effect on LPL activity, the mediation on glucose homeostasis or the effect on leptin. To assess the role of TNFalpha in obesity we measured adipocyte TNFalpha expression in 96 females with a wide range of adiposity and with or without type 2 diabetes. We analysed the relationship between TNFalpha expression, adipocyte LPL activity, insulin resistance and leptin in this population. RESULTS: The TNFalpha and leptin expression of the adipose tissue in obese and morbid obese patients were significantly higher than in controls. Obese and morbid obese patients had slightly higher levels of LPL activity, but these differences were not significant. We observed a significant relationship between adipose TNFalpha expression and body mass index (r=0.35, P < 0.001). TNFalpha expression was negatively related to LPL activity (r= -0.28, P < 0.05) and positively related to leptin expression (r=0.35, P < 0.001). CONCLUSION: Our results indicate that obese women, even those with morbid obesity, over-express TNFalpha in subcutaneous adipose tissue in proportion to the magnitude of the fat depot and independently of the presence of type 2 diabetes. The TNFalpha system may be a homeostatic mechanism that prevents further fat deposition by regulating LPL activity and leptin production.
引用
收藏
页码:652 / 658
页数:7
相关论文
共 43 条
[1]   STABILIZATION OF THE BIOACTIVITY OF TUMOR-NECROSIS-FACTOR BY ITS SOLUBLE RECEPTORS [J].
ADERKA, D ;
ENGELMANN, H ;
MAOR, Y ;
BRAKEBUSCH, C ;
WALLACH, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1992, 175 (02) :323-329
[2]  
American Diabetes Association, 1998, DIABETES CARE S1, V21, ps5
[3]  
Bemelmans MHA, 1996, CRIT REV IMMUNOL, V16, P1
[4]   Tumour necrosis factor, a key role in obesity? [J].
Bulló-Bonet, M ;
García-Lorda, P ;
López-Soriano, FJ ;
Argilés, JM ;
Salas-Salvadó, J .
FEBS LETTERS, 1999, 451 (03) :215-219
[5]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[6]   CHANGES IN THERMOGENESIS AND BROWN FAT ACTIVITY IN RESPONSE TO TUMOR NECROSIS FACTOR IN THE RAT [J].
COOMBES, RC ;
ROTHWELL, NJ ;
SHAH, P ;
STOCK, MJ .
BIOSCIENCE REPORTS, 1987, 7 (10) :791-799
[7]   Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects [J].
Corica, F ;
Allegra, A ;
Corsonello, A ;
Buemi, M ;
Calapai, G ;
Ruello, A ;
Mauro, VN ;
Ceruso, D .
INTERNATIONAL JOURNAL OF OBESITY, 1999, 23 (04) :355-360
[8]   Tumor necrosis factor-α inhibits leptin production in subcutaneous and omental adipocytes from morbidly obese humans [J].
Fawcett, RL ;
Waechter, AS ;
Williams, LB ;
Zhang, PL ;
Louie, R ;
Jones, R ;
Inman, M ;
Huse, J ;
Considine, RV .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (02) :530-535
[9]  
Foz M., 2000, MED CLIN-BARCELONA, V115, P587, DOI [10.1016/S0025-7753(00)71632-0, DOI 10.1016/S0025-7753(00)71632-0]
[10]  
FRIED SK, 1989, J LIPID RES, V30, P1917