title: Adipocytokines and the metabolic syndrome among older persons with and without obesity: the InCHIANTI study.
abstract: OBJECTIVE
  Adipose tissue-derived inflammation may contribute to metabolic alterations and eventually to the metabolic syndrome (MetS). The purpose of this study was to: (1) examine the role of adipocytokines in the association between obesity and the MetS and (2) to determine whether the association is different in obese and non-obese persons.
  
  
  METHODS
  Cross-sectional population-based InCHIANTI study.
  
  
  METHODS
  A total of 944 community-dwelling adults aged 65 years and older living in Tuscany, Italy.
  
  
  METHODS
  Obesity was defined as body mass index > or =30 kg/m2 and MetS as > or =3 of the ATP-III criteria. Circulating levels of C-reactive protein, interleukin (IL)-6, IL-1 receptor antagonist (IL-1ra), IL-18, tumour necrosis factor (TNF)-alpha R1, adiponectin, resistin and leptin were measured. Additionally, insulin resistance was determined using the homeostasis model assessment (HOMA-IR).
  
  
  RESULTS
  The prevalence of the MetS was 32%. Both overall and abdominal obesity were significantly associated with the MetS after adjusting for inflammatory cytokines, adipokines and lifestyle factors. After adjusting for multiple confounders and HOMA-IR, IL-1ra, TNF-alpha R1 and adiponectin (P < 0.05) remained significantly associated with the MetS. Having multiple cytokines in the highest tertile increased the likelihood of having the MetS in both obese (P for trend 0.002) and non-obese persons (P for trend 0.001) independent of insulin resistance.
  
  
  CONCLUSIONS
  Non-obese and obese individuals who develop an intense pro-inflammatory state may be more prone to develop the MetS than those with lower levels of inflammation.
authors.affiliation: Clinical Research Branch, National Institute on Aging, 3001 S. Hanover Street, Baltimore, MD 21225, USA. stenholmsm@mail.nih.gov
authors.forename: Sari
authors.initials: S
authors.lastname: Stenholm
authors.forename: Annemarie
authors.initials: A
authors.lastname: Koster
authors.forename: Dawn E
authors.initials: DE
authors.lastname: Alley
authors.forename: Marjolein
authors.initials: M
authors.lastname: Visser
authors.forename: Marcello
authors.initials: M
authors.lastname: Maggio
authors.forename: Tamara B
authors.initials: TB
authors.lastname: Harris
authors.forename: Josephine M
authors.initials: JM
authors.lastname: Egan
authors.forename: Stefania
authors.initials: S
authors.lastname: Bandinelli
authors.forename: Jack M
authors.initials: JM
authors.lastname: Guralnik
authors.forename: Luigi
authors.initials: L
authors.lastname: Ferrucci
mesh_terms: D054392:Adipokines / Q000502:physiology*; D052242:Adiponectin / Q000097:blood; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D053590:Interleukin 1 Receptor Antagonist Protein / Q000097:blood; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000503:physiopathology*; D056128:Obesity, Abdominal / Q000150:complications / Q000503:physiopathology*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D052243:Resistin / Q000097:blood
chemical_list: D054392:Adipokines; D052242:Adiponectin; D053590:Interleukin 1 Receptor Antagonist Protein; D020382:Interleukin-18; D015850:Interleukin-6; D020738:Leptin; D047888:Receptors, Tumor Necrosis Factor, Type I; D052243:Resistin; D002097:C-Reactive Protein