title: Lipopolysaccharide-binding protein plasma levels in children: effects of obstructive sleep apnea and obesity.
abstract: BACKGROUND
  Obstructive sleep apnea (OSA) has been linked to obesity, inflammation, and metabolic syndrome. The gut microbiota, which serves as reservoir for bacterial lipopolysaccharides (LPS), could be altered by OSA and trigger inflammation. LPS-binding protein (LBP) serves as a surrogate marker of underlying low-grade endotoxemia by LPS from the gut. We hypothesized that systemic LBP levels would be higher in obese children and in those with OSA.
  
  
  METHODS
  Consecutive snoring and nonsnoring children (mean age 6.8 ± 1.3 y) were included after overnight polysomnography, and fasting levels of lipids, insulin glucose, and high-sensitivity C-reactive protein were obtained. Children were subdivided into four subgroups based on the presence of obesity or OSA. Plasma LBP levels were assayed using ELISA.
  
  
  RESULTS
  Of 219 participants, nonobese controls had the lowest levels of LBP, and the presence of obesity without OSA was associated with significant LBP increases. Nonobese children with OSA exhibited increased LBP levels, with obese children with OSA demonstrating the highest LBP levels of all four groups. Furthermore, LBP was independently associated with body mass index and with measures of OSA severity as well as with metabolic dysfunction, particularly insulin resistance as indicated by the homeostasis model assessment of insulin resistance.
  
  
  CONCLUSIONS
  Systemic low-level endotoxemia and resultant systemic inflammation is present in children who are either obese or suffer from OSA and is particularly prominent when both conditions are present. We postulate that disrupted sleep and other factors facilitating obesity such as a high-fat diet may disrupt the gut microbiome and lead to increased systemic LPS levels with resultant inflammation, promoting downstream metabolic dysfunction.
authors.affiliation: Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Chicago, Illinois 60637.
authors.forename: Leila
authors.initials: L
authors.lastname: Kheirandish-Gozal
authors.forename: Eduard
authors.initials: E
authors.lastname: Peris
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Maximiliano
authors.initials: M
authors.lastname: Tamae Kakazu
authors.forename: Abdelnaby
authors.initials: A
authors.lastname: Khalyfa
authors.forename: Alba
authors.initials: A
authors.lastname: Carreras
authors.forename: David
authors.initials: D
authors.lastname: Gozal
mesh_terms: D000209:Acute-Phase Proteins; D015992:Body Mass Index; D002352:Carrier Proteins / Q000097:blood*; D002648:Child; D005260:Female; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D017286:Polysomnography; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein