title: The role of serum adipocyte fatty acid-binding protein on the development of metabolic syndrome is independent of pro-inflammatory cytokines.
abstract: OBJECTIVE
  Adipocyte fatty acid-binding protein (FABP4) is abundantly expressed in adipocytes and plays a role in glucose homeostasis. We analysed the relationship between serum FABP4 levels and the progression of metabolic syndrome in healthy adults.
  
  
  RESULTS
  A total of 465 subjects were selected from participants in a medical check-up programme at a Health Promotion Center. Baseline serum FABP4 levels were measured, and the subjects were evaluated for the presence of metabolic syndrome (MetS) according to the recommendations of the American Heart Association/National Heart, Lung, and Blood Institute. The subjects were re-evaluated 4 years later. Baseline FABP4 concentrations were significantly higher in subjects with MetS than in those without MetS (P<0.001). At the 4-year follow-up, subjects in the highest FABP4 tertile at baseline exhibited higher values for body mass index, fat mass and percent body fat, as well as blood pressure, fasting glucose, total cholesterol, triglycerides, low-density lipoprotein (LDL)-cholesterol, insulin, homeostasis model assessment of insulin resistance, monocyte chemoattractant protein-1 and tumor necrosis factor-α levels (all P<0.05). The subjects with higher FABP4 levels had lower HDL-cholesterol concentrations (P<0.05). After adjustment for age, sex, change in percent body fat and baseline values for other metabolic and inflammatory parameters, FABP4 levels at baseline were shown to be strongly associated with the development of MetS by year 4 (odds ratio (OR), 5.75; 95% confidence interval (CI), 2.71-12.23 for highest tertile vs. lowest tertile, P<0.001)
  
  
  CONCLUSIONS
  Baseline serum FABP4 levels appear to be a significant predictor for the future development of MetS, independent of pro-inflammatory cytokines.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, No. 108 Pyung-Dong, Jongro-Ku, Seoul 110-746, Republic of Korea.
authors.forename: S E
authors.initials: SE
authors.lastname: Park
authors.forename: E-J
authors.initials: EJ
authors.lastname: Rhee
authors.forename: W-Y
authors.initials: WY
authors.lastname: Lee
authors.forename: W-J
authors.initials: WJ
authors.lastname: Kim
authors.forename: S-H
authors.initials: SH
authors.lastname: Yoo
authors.forename: J-C
authors.initials: JC
authors.lastname: Bae
authors.forename: E-S
authors.initials: ES
authors.lastname: Choi
authors.forename: C-Y
authors.initials: CY
authors.lastname: Park
authors.forename: K-W
authors.initials: KW
authors.lastname: Oh
authors.forename: S-W
authors.initials: SW
authors.lastname: Park
authors.forename: S-W
authors.initials: SW
authors.lastname: Kim
mesh_terms: D017667:Adipocytes / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D016207:Cytokines / Q000097:blood; D005215:Fasting; D050556:Fatty Acid-Binding Proteins / Q000097:blood*; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000503:physiopathology; D008875:Middle Aged; D011446:Prospective Studies; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D001786:Blood Glucose; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D016207:Cytokines; C493410:FABP4 protein, human; D050556:Fatty Acid-Binding Proteins; D007328:Insulin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha