title: Insulin resistance can impair reduction on carotid intima-media thickness in obese adolescents.
abstract: BACKGROUND
  The atherosclerotic process at the endothelial level begins in early ages and seems to be associated with obesity and its comorbidities as insulin resistance.
  
  
  OBJECTIVE
  The aim of this study was to verify the influence of insulin resistance on inflammatory and subclinical markers of atherosclerosis in obese adolescents.
  
  
  METHODS
  Sixty-six post-pubescent obese adolescents were divided in two groups according to homeostasis model assessment of insulin resistance (HOMA-IR) measurement: with insulin resistance (IR) n=39 and without insulin resistance (NIR) n=27, and submitted to an interdisciplinary intervention over the course of 1 year. Common carotid artery intima-media thickness (cIMT), visceral and subcutaneous adipose tissue was determined by ultrasound. Body composition, blood pressure, HOMA-IR, lipid profile and adipokines concentrations [leptin, adiponectin, and plasminogen activator inhibitor type (PAI-1)] were analyzed before and after the therapy.
  
  
  RESULTS
  Both groups presented significant improvements in body composition, inflammatory state (reduction of leptin and PAI-1 concentration; increasing of plasma adiponectin) and reduction of cIMT. Only NIR group showed positive correlation between changes in visceral fat (∆Visceral) and changes in cIMT (∆ cIMT) (r = 0.42; p < 0.05). Simple linear regression analyze revealed ∆Visceral to be an independent predictor to reduction of cIMT in this group (R2 adjusted = 0.14, p = 0.04). The final values of cIMT remained significantly higher in IR group when compared to NIR group.
  
  
  CONCLUSIONS
  The presence of insulin resistance can impair changes in cIMT leading to early development of atherosclerosis in obese adolescents submitted to an interdisciplinary intervention..
authors.affiliation: Universidade Federal de São Paulo, São Paulo, UNIFESP, SP, Brasil.
authors.forename: Priscila de Lima
authors.initials: Pde L
authors.lastname: Sanches
authors.forename: Marco Túlio de
authors.initials: MT
authors.lastname: Mello
authors.forename: Francisco Antonio Helfestein
authors.initials: FA
authors.lastname: Fonseca
authors.forename: Natália
authors.initials: N
authors.lastname: Elias
authors.forename: Aline de
authors.initials: Ad
authors.lastname: Piano
authors.forename: June
authors.initials: J
authors.lastname: Carnier
authors.forename: Lian
authors.initials: L
authors.lastname: Tock
authors.forename: Lila Missae
authors.initials: LM
authors.lastname: Oyama
authors.forename: Sergio
authors.initials: S
authors.lastname: Tufik
authors.forename: Ana
authors.initials: A
authors.lastname: Dâmaso
mesh_terms: D054392:Adipokines / Q000097:blood; D000293:Adolescent; D000704:Analysis of Variance; D000886:Anthropometry; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002340:Carotid Artery Diseases / Q000209:etiology / Q000503:physiopathology*; D059168:Carotid Intima-Media Thickness; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012307:Risk Factors; D018709:Statistics, Nonparametric; D055815:Young Adult
chemical_list: D054392:Adipokines; D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1