Relations among Adiposity and Insulin Resistance with Flow-Mediated Dilation, Carotid Intima-Media Thickness, and Arterial Stiffness in Children

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Abstract

Objective To determine the associations of adiposity and insulin resistance with measures of vascular structure and function in children. Study design A cross-sectional study included 252 children (age 15.1 ± 2.4 years; body mass index percentile 68.2 ± 26.5%; Tanner 2-5). Measurements of body fat percentage were obtained with dual-energy X-ray absorptiometry and visceral adipose tissue (VAT) with computed tomography. Insulin resistance was measured with hyperinsulinemic euglycemic clamp. Vascular measurements for endothelial function (brachial artery flow-mediated dilation [FMD]), vascular structure (carotid intima-media thickness [cIMT]), vascular stiffness (carotid incremental elastic modulus), and pulse wave velocity were analyzed by tertiles of adiposity and insulin resistance. Additional analyses with ANCOVA and linear regression were adjusted for Tanner, sex, race, and family relationship; FMD was also adjusted for baseline artery diameter. Results FMD was positively associated with high adiposity (body mass index, body fat percentage, and VAT) (P <.01 all). Insulin resistance was not associated with FMD. cIMT was significantly, positively related to obesity, VAT, and insulin resistance (P <.05 all). No differences in carotid incremental elastic modulus and pulse wave velocity were observed in relation to adiposity or insulin resistance. Conclusions The findings suggest that adiposity is associated with higher FMD, and insulin resistance and VAT are associated with higher cIMT in children. Further research is needed to clarify the progression of these relations.

Original languageEnglish (US)
Pages (from-to)205-211
Number of pages7
JournalJournal of Pediatrics
Volume168
DOIs
StatePublished - Jan 1 2016

Bibliographical note

Funding Information:
Funded by the National Institutes of Health (NIH)/ National Institute of Diabetes and Digestive and Kidney Diseases (IDDK) ( R01-DK072124-01A3 [to J.S.] and T32-DK083250 [to J.R.]), National Cancer Institute / NIDDK ( R01CA113930-01A1 [to J.S.]), General Clinical Research Center Program ( M01-RR00400 ), National Center for Research Resources ( 1UL1-RR033183 ), the Clinical and Translational Science Institute at the University of Minnesota-Twin Cities ( UL1TR000114 ), and NIH / National Heart, Lung, and Blood Institute ( F32-HL127851-01 [to J.R.]). A.K. has served on pediatric obesity advisory boards for Takeda and Novo Nordisk (unpaid). The other authors declare no conflicts of interest.

Funding Information:
Funded by the National Institutes of Health (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases (IDDK) (R01-DK072124-01A3 [to J.S.] and T32-DK083250 [to J.R.]), National Cancer Institute/NIDDK (R01CA113930-01A1 [to J.S.]), General Clinical Research Center Program (M01-RR00400), National Center for Research Resources (1UL1-RR033183), the Clinical and Translational Science Institute at the University of Minnesota-Twin Cities (UL1TR000114), and NIH/National Heart, Lung, and Blood Institute (F32-HL127851-01 [to J.R.]). A.K. has served on pediatric obesity advisory boards for Takeda and Novo Nordisk (unpaid). The other authors declare no conflicts of interest. We would like to thank all of the children who participated in this study.

Publisher Copyright:
© 2016 Elsevier Inc.

Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.

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