title: Relationships of cardiac autonomic function with metabolic abnormalities in childhood obesity.
abstract: OBJECTIVE
  The objective was to examine cardiovascular autonomic (cANS) function and its potential relationships with leptin resistance, insulin resistance, oxidative stress, and inflammation in a pediatric sample with varying levels of obesity.
  
  
  METHODS
  Participants were normal-weight (NW; BMI <85th percentile, 6 male, 4 female), overweight (OW; 85th percentile < BMI <95th percentile, 6 male, 4 female), and obese children (OB; BMI >95th percentile, 6 male, 10 female) who had cANS function assessed via heart rate variability (HRV) methods during resting conditions. Standard time-domain and frequency-domain measures [high-frequency normalized units (HFnu; measure of parasympathetic nervous system activity) and low frequency:high-frequency ratio (LF:HF; overall sympathovagal balance)] of HRV were calculated. Fasting blood samples were drawn for measurement of glucose, insulin, lipids, 8-isoprostane, leptin, soluble leptin-receptor (sOB-R), C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Results were reported as mean +/- standard error of the mean.
  
  
  RESULTS
  OB had significantly elevated LF:HF and decreased HFnu when compared with NW (p < 0.05), but no differences between OW and NW were observed. Measures of HRV were significantly related to leptin, insulin resistance, 8-isoprostane, and CRP (p < 0.05), but these relationships were not significant after adjustment for fat mass.
  
  
  CONCLUSIONS
  When compared with NW, OB but not OW children are characterized by cANS dysfunction and increased leptin, insulin resistance, oxidative stress, and inflammation (CRP). The relationships between these factors seem to be dependent on quantity of fat mass and/or other factors associated with being obese.
authors.affiliation: School of Kinesiology, University of Minnesota, Minneapolis, MN 55102, USA. kauf0127@umn.edu
authors.forename: Christopher L
authors.initials: CL
authors.lastname: Kaufman
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Kaiser
authors.forename: Julia
authors.initials: J
authors.lastname: Steinberger
authors.forename: Aaron S
authors.initials: AS
authors.lastname: Kelly
authors.forename: Donald R
authors.initials: DR
authors.lastname: Dengel
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D005260:Female; D006321:Heart / Q000502:physiology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006331:Heart Diseases / Q000453:epidemiology; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D008659:Metabolic Diseases / Q000150:complications / Q000503:physiopathology*; D008910:Minnesota / Q000453:epidemiology; D009765:Obesity / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology*; D012016:Reference Values; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein