PMID- 17608757
OWN - NLM
STAT- MEDLINE
DCOM- 20080430
LR  - 20071023
IS  - 0300-0664 (Print)
IS  - 0300-0664 (Linking)
VI  - 67
IP  - 5
DP  - 2007 Nov
TI  - Effect of weight loss induced by gastric bypass on proinflammatory 
      interleukin-18, soluble tumour necrosis factor-alpha receptors, C-reactive 
      protein and adiponectin in morbidly obese patients.
PG  - 679-86
AB  - OBJECTIVE: Interleukin-18 (IL-18) is a potent proinflammatory cytokine whose role 
      in human obesity has recently been suggested. The aim of our study was to analyse 
      in morbidly obese patients undergoing gastric bypass, the relationship of IL-18 
      with insulin resistance and with proinflammatory cytokines (tumour necrosis 
      factor-alpha receptors, sTNFR), C-reactive protein (CRP) and with adiponectin. 
      DESIGN: Observational and prospective study. PATIENTS: Sixty-five morbidly obese 
      patients, aged 45 +/- 8.9 years, were studied before and 12 months after gastric 
      bypass. MEASUREMENTS: We analysed plasma concentrations of IL-18, sTNFR, CRP and 
      adiponectin. RESULTS: Plasma concentrations of sTNFR2, IL-18 and CRP were 
      decreased and adiponectin significantly increased after bypass surgery. In the 
      multiple regression analysis, preoperative values of IL-18 remained significantly 
      associated with preoperative triglycerides (beta = 0.47, P = 0.005) and TNFR2 
      (beta = 0.47, P = 0.004). R(2) for the model = 0.38. Postoperative IL-18 
      concentrations in the multiple regression analysis were significantly associated 
      with postoperative homeostasis model assessment of insulin resistance (HOMA-IR) 
      (beta = 0.092, P = 0.019) and triglycerides (beta = 0.40, P = 0.036). R(2) for 
      the model = 0.46. IL-18 did not correlate with body mass index, fat mass, 
      fat-free mass or body fat. No relationship was either found between adiponectin 
      and IL-18, TNFR1 and -2 and CRP. CONCLUSIONS: Massive weight loss induced by 
      gastric bypass reduces IL-18, TNFR2 and CRP. IL-18 might be a marker of the 
      chronic inflammatory process underlying insulin resistance but its lack of 
      association with anthropometric and body composition parameters does not support 
      a major secretion by human adipocytes. IL-18 and sTNFR1 and -2 do not play a main 
      role in the inhibition of the secretion of adiponectin.
FAU - Vilarrasa, N
AU  - Vilarrasa N
AD  - Endocrinology and Diabetes Unit, Hospital Universitari de Bellvitge, Barcelona, 
      Spain. nuriavilarrasa@yahoo.es
FAU - Vendrell, J
AU  - Vendrell J
FAU - Sanchez-Santos, R
AU  - Sanchez-Santos R
FAU - Broch, M
AU  - Broch M
FAU - Megia, A
AU  - Megia A
FAU - Masdevall, C
AU  - Masdevall C
FAU - Gomez, N
AU  - Gomez N
FAU - Soler, J
AU  - Soler J
FAU - Pujol, J
AU  - Pujol J
FAU - Bettonica, C
AU  - Bettonica C
FAU - Aranda, H
AU  - Aranda H
FAU - Gomez, J M
AU  - Gomez JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070702
PL  - England
TA  - Clin Endocrinol (Oxf)
JT  - Clinical endocrinology
JID - 0346653
RN  - 0 (Adiponectin)
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Interleukin-18)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Adiponectin/*blood
MH  - Adult
MH  - C-Reactive Protein/*analysis
MH  - Cholesterol, HDL/blood
MH  - Cholesterol, LDL/blood
MH  - Female
MH  - *Gastric Bypass
MH  - Humans
MH  - Interleukin-18/*blood
MH  - Male
MH  - Middle Aged
MH  - *Obesity, Morbid/blood/immunology/surgery
MH  - Prospective Studies
MH  - Receptors, Tumor Necrosis Factor/*blood
MH  - Receptors, Tumor Necrosis Factor, Type I/blood
MH  - Receptors, Tumor Necrosis Factor, Type II/blood
MH  - Regression Analysis
MH  - Weight Loss
EDAT- 2007/07/05 09:00
MHDA- 2008/05/01 09:00
CRDT- 2007/07/05 09:00
PHST- 2007/07/05 09:00 [pubmed]
PHST- 2008/05/01 09:00 [medline]
PHST- 2007/07/05 09:00 [entrez]
AID - CEN2945 [pii]
AID - 10.1111/j.1365-2265.2007.02945.x [doi]
PST - ppublish
SO  - Clin Endocrinol (Oxf). 2007 Nov;67(5):679-86. doi: 
      10.1111/j.1365-2265.2007.02945.x. Epub 2007 Jul 2.