title: Insulin resistance, leptin and TNF-alpha system in morbidly obese women after gastric bypass.
abstract: Obesity is a complex disease associated with insulin resistance. Leptin and the TNF-alpha system could be involved in the pathogenesis of obesity and insulin resistance. Gastric bypass (GBP) is a surgical treatment for morbidly obese patients. We conducted a study after GBP to analyze the pattern of variation of anthropometric and body composition variables, leptin and sTNFR1 and 2.
  
  
  METHODS
  29 morbidly obese women were studied, at baseline and throughout 6 months after gastric bypass.
  
  
  RESULTS
  At baseline, the BMI was 49 +/- 6 kg/m(2) and patients showed a higher fasting insulin resistance index (FIRI), leptin, leptin/fat mass and sTNFR1 and 2 than did controls. 6 months after GBP, BMI was 35+/-4, and FIRI, leptin and leptin/fat mass decreased significantly in the first months and throughout the follow-up. sTNFR1 and 2 showed an initial increase, but at 6 months their concentrations were similar to baseline (2.6+/-0.8 vs 3.1+/-0.95 ng/ml, P < 0.05; 4.6+/-1.4 vs 7+/-2.5 ng/ml, P < 0.05). At baseline, there was no correlation between leptin and BMI and body composition variables but there was a correlation with fat mass (r=0.42, P=0.004) and sTNFR1 (r=0.58, P=0.001). At 6 months, there was a correlation between leptin and BMI (r=0.53, P=0.004) and sTNFR1 (r=0.46, P=0.013).
  
  
  CONCLUSIONS
  Morbidly obese women after GBP became less insulin resistant with lower leptin concentrations, but showed an initial increase of sTNFR1 and 2. This pattern of variation of the leptin TNF-alpha axis suggests a disregulation of the system after dramatic weight loss and also that insulin and leptin up-regulate TNF-alpha production irrespective of insulin resistance status.
authors.affiliation: Department of Endocrinology, Prínceps d'Espanya Hospital, Barcelona, Spain. 30903xrc@comb.es
authors.forename: Ana
authors.initials: A
authors.lastname: Molina
authors.forename: Joan
authors.initials: J
authors.lastname: Vendrell
authors.forename: Cristina
authors.initials: C
authors.lastname: Gutiérrez
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Simón
authors.forename: C
authors.initials: C
authors.lastname: Masdevall
authors.forename: Juan
authors.initials: J
authors.lastname: Soler
authors.forename: José Manuel
authors.initials: JM
authors.lastname: Gómez
mesh_terms: D000328:Adult; D000886:Anthropometry; D015703:Antigens, CD / Q000097:blood; D001823:Body Composition / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D015390:Gastric Bypass; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D020738:Leptin / Q000097:blood*; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood* / Q000150:complications / Q000601:surgery*; D017063:Outcome Assessment, Health Care; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D013997:Time Factors
chemical_list: D015703:Antigens, CD; C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II