title: Systemic inflammation, adipose tissue tumor necrosis factor, and leptin expression.
abstract: OBJECTIVE
  To explore the links between tumor necrosis factor alpha (TNFalpha) and leptin adipose tissue expression and low-grade systemic inflammation and to determine the relationship between inflammation and the degree of adiposity, the presence of type 2 diabetes, and other cardiovascular risk factors.
  
  
  METHODS
  Ninety-one women (BMI 19 to 65 kg/m(2)) were divided into tertiles of CRP. Insulin resistance was calculated using the HOMA method. Albumin, fibrinogen, C-reactive protein (CRP), interleukin-6, sTNFR1, sTNFR2, and leptin levels were measured in serum and plasma samples. TNFalpha and leptin expression were measured by reverse transcription-polymerase chain reaction in abdominal subcutaneous adipose tissue samples.
  
  
  RESULTS
  CRP was positively related to BMI and upper distribution of adiposity. TNFalpha and leptin adipose tissue expression were higher in the upper tertile of CRP. Also, peripheral levels of both soluble TNFRs and leptin were higher in patients with the greatest inflammation degree. Diabetes, dislipidemia, and hypertension were most prevalent in patients in the upper CRP tertile. Inflammatory markers of diabetic women were significantly different from those of nondiabetic women, even after adjusting for differences in body fat. BMI, type 2 diabetes, and adipose TNFalpha mRNA levels were significant predictors of serum CRP levels (r(2) = 0.28, p < 0.001).
  
  
  CONCLUSIONS
  These results are in agreement with the hypothesis that the synthesis of adipose tissue TNFalpha and leptin could induce the production of interleukin-6, CRP, and other acute-phase reactants, thus contributing to the maintenance of chronic low-grade inflammation state involved in the progression of obesity and its associated comorbidities.
authors.affiliation: Unitat de Nutrició Humana, Facultat de Medicina i Ciències de la Salut de Reus, Universitat Rovira i Virgili, Reus, Spain.
authors.forename: Monica
authors.initials: M
authors.lastname: Bulló
authors.forename: Pilar
authors.initials: P
authors.lastname: García-Lorda
authors.forename: Isabel
authors.initials: I
authors.lastname: Megias
authors.forename: Jordi
authors.initials: J
authors.lastname: Salas-Salvadó
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry*; D000328:Adult; D015703:Antigens, CD / Q000097:blood; D001823:Body Composition; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood / Q000235:genetics*; D007958:Leukocyte Count; D012333:RNA, Messenger / Q000032:analysis; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D015703:Antigens, CD; D015850:Interleukin-6; C515448:LEPR protein, human; D020738:Leptin; D012333:RNA, Messenger; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein