Overweight and hyperinsulinemia provide individual contributions to compromises in brachial artery distensibility in healthy adolescents and young adults


Journal Article

Brachial artery distensibility (BrachD) was measured in healthy children to identify associations with atherosclerotic risk factors. Nine hundred sixty-nine black and white subjects, 13-22 years of age, were classified as lean (L) or overweight (O) and as hyperinsulinemic (H-I) or normoinsulinemic (N-I). Blood pressure (BP) and BrachD were obtained with a DynaPulse Pathway instrument. Analysis of variance was performed, looking for group mean differences. Correlations between BrachD and risk variables were examined. Determinates of BrachD were determined by backward elimination regression, stratified by body mass index (BMI)-insulin group. Decreased BrachD correlated with male gender, O, higher BP, heart rate, fasting glucose, and log of fasting insulin after adjusting for pulse pressure (PP). BrachD was greatest in L+N-I, with progressive decreases seen in L+H-I, O+N-I, and O+H-I subjects. Regression modeling found that PP and HR were major determinates of BrachD. Glucose was significant for subjects with N-I, regardless of adiposity. Excluding BP, glucose remained important in N-I subjects. Gender was significant for all. HR retained significance only in O subjects, regardless of insulin level. In healthy adolescents, hyperinsulinemia and obesity adversely affect brachial artery function, with overweight contributing to a greater degree. In normoinsulinemic subjects, fasting glucose was inversely related to BrachD. Metabolic factors may play a role in vascular function in youth. © 2007 American Society of Hypertension.

Full Text

Duke Authors

Cited Authors

  • Urbina, EM; Bean, JA; Daniels, SR; D'Alessio, D; Dolan, LM

Published Date

  • May 1, 2007

Published In

Volume / Issue

  • 1 / 3

Start / End Page

  • 200 - 207

International Standard Serial Number (ISSN)

  • 1933-1711

Digital Object Identifier (DOI)

  • 10.1016/j.jash.2007.01.008

Citation Source

  • Scopus