title: TNFalpha expression of subcutaneous adipose tissue in obese and morbid obese females: relationship to adipocyte LPL activity and leptin synthesis.
abstract: BACKGROUND
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Unitat de Nutrició Humana, Facultat de Medicina i Ciències de la Salut de Reus, Universitat Rovira i Virgili, Reus, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Bulló
authors.forename: P
authors.initials: P
authors.lastname: García-Lorda
authors.forename: J
authors.initials: J
authors.lastname: Peinado-Onsurbe
authors.forename: M
authors.initials: M
authors.lastname: Hernández
authors.forename: D
authors.initials: D
authors.lastname: Del Castillo
authors.forename: J M
authors.initials: JM
authors.lastname: Argilés
authors.forename: J
authors.initials: J
authors.lastname: Salas-Salvadó
mesh_terms: D017667:Adipocytes / Q000201:enzymology / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000293:Adolescent; D000328:Adult; D000368:Aged; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003920:Diabetes Mellitus / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000096:biosynthesis* / Q000235:genetics; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D009767:Obesity, Morbid / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D008071:Lipoprotein Lipase