title: Impact of weight loss on inflammatory proteins and their association with the insulin resistance syndrome in morbidly obese patients.
abstract: OBJECTIVE
  Obesity is closely linked to the insulin resistance syndrome (IRS), type 2 diabetes, and cardiovascular disease, the primary cause of morbidity and mortality in these patients. Elevated levels of C-reactive protein (CRP) and interleukin-6 (IL-6), indicating chronic subclinical inflammation, have been associated with features of the IRS and incident cardiovascular disease.
  
  
  RESULTS
  We studied the cross-sectional and longitudinal relation of CRP, IL-6, and tumor necrosis factor-alpha (TNF-alpha) with features of the IRS in 37 morbidly obese patients with different stages of glucose tolerance before and 14 months after gastric surgery. Weight loss after gastric surgery induced a significant shift from diabetes (37% vs 3%) to impaired glucose tolerance (40% vs 33%) and normal glucose tolerance (23% vs 64%). The baseline concentration of IL-6 was correlated with TNF-alpha (r=0.59, P<0.01) and CRP (r=0.44, P<0.05) levels. TNF-alpha, IL-6, and CRP were significantly correlated with insulin resistance estimated by the homeostatic model assessment (r=0.48, P<0.05; r=0.56, P<0.01; and r=0.35, P<0.05, respectively). Concentrations of CRP and IL-6 decreased after weight loss (median, 8.6 and interquartile range, 2.7/14.5 vs 2.5 and 1.2/4.1 mg/L; P<0.006, and 5.13 and 2.72/12.15 vs 3.95 and 1.97/5.64 pg/mL, P<0.02, respectively), whereas serum levels of TNF-alpha remained unchanged (8.6 and 6.3/18.8 vs 11.7 and 5.8/17.2 pg/mL; NS.). Multiple regression analysis revealed that the decrease in insulin resistance remained independently and significantly correlated with the decrease in IL-6 concentrations (P<0.01) and the decrease in body mass index with the decrease in CRP (P<0.05), respectively.
  
  
  CONCLUSIONS
  Weight loss in morbidly obese patients induces a significant decrease of CRP and IL-6 concentrations in association with an improvement of the IRS.
authors.affiliation: Department of Medicine 1, Rudolfstiftung Hospital, Juchgasse 25, A-1030 Vienna, Austria. Hans-Peter.Kopp@kar.magwien.gv.at
authors.forename: H P
authors.initials: HP
authors.lastname: Kopp
authors.forename: C W
authors.initials: CW
authors.lastname: Kopp
authors.forename: A
authors.initials: A
authors.lastname: Festa
authors.forename: K
authors.initials: K
authors.lastname: Krzyzanowska
authors.forename: S
authors.initials: S
authors.lastname: Kriwanek
authors.forename: E
authors.initials: E
authors.lastname: Minar
authors.forename: R
authors.initials: R
authors.lastname: Roka
authors.forename: G
authors.initials: G
authors.lastname: Schernthaner
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D015391:Gastroplasty; D006801:Humans; D007249:Inflammation / Q000097:blood*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood*; D008055:Lipids / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000097:blood* / Q000150:complications / Q000601:surgery; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*; D015431:Weight Loss
chemical_list: D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha; D005340:Fibrinogen; D002097:C-Reactive Protein