Circulating activated endothelial cells in pediatric obesity

Aaron S Kelly, Robert P Hebbel, Anna Solovey, Sarah J Schwarzenberg, Andrea M. Metzig, Antoinette Moran, Alan R Sinaiko, David R Jacobs Jr, Julia Steinberger

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22 Scopus citations

Abstract

Objective: We characterized the state of the vascular endothelium in pediatric obesity by comparing circulating endothelial cell (CEC) number and activation phenotype in severely obese children to that of normal weight, overweight, and obese children. Study design: We used immunohistochemical examination of buffy-coat smears to enumerate CEC and immunofluorescence microscopy to quantify activated CEC in 107 children and adolescents. Normal weight (body mass index [BMI] <85th percentile; n = 40), overweight (BMI 85th-<95th percentile; n = 17), and obese (BMI 95th-<99th percentile; n = 23) participants were recruited from a longitudinal study. Severely obese (BMI ≥99th percentile; n = 27) participants were recruited from a pediatric obesity clinic. Group means (adiposity; systolic blood pressure [SBP] quartiles) were compared with general linear models, adjusted for sex, age, and race. With Pearson correlations, we characterized relations of CEC with cardiovascular risk factors. Results: Activated CEC increased across BMI groups (P < .002) and SBP quartiles (P < .05). CEC number and activated CEC were highest in the severely obese group. CEC number was significantly associated with SBP, diastolic blood pressure, and triglycerides level. Activated CEC were significantly associated with SBP and high-density lipoprotein cholesterol levels. Conclusions: The vascular endothelium was activated in relation to excess adiposity, particularly in severely obese children, and to elevated SBP in children and adolescents.

Original languageEnglish (US)
Pages (from-to)547-551
Number of pages5
JournalJournal of Pediatrics
Volume157
Issue number4
DOIs
StatePublished - Oct 2010

Bibliographical note

Funding Information:
Funding was provided in part by University of Minnesota Vikings Children's Fund (A.K.), Minnesota Medical Foundation (A.K.), National Institutes of Health ( P01 HL55552 to R.H.), National Institutes of Health ( 1RO1DK072124-01A3 to J.S.), and GCRC ( M01-RR00400 ), General Clinical Research Center Program, NCRR/NIH . The authors declare no conflicts of interest.

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