ARTERIAL DYSFUNCTION IN PEDIATRIC PATIENTS WITH IMPAIRED FASTING GLUCOSE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Cardiovascular disease (CVD) is the leading cause of death worldwide and Type 2 diabetes mellitus (T2DM) increases the risk of death from CVD by 5 to 7 times. Pre-diabetes, defined as a state of either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT), is associated with an increased risk of CVD. The CVD risk in pre-diabetes remains elevated even in the large percentage of patients who never go on to develop type 2 diabetes. While recent data have largely been generated from adult research studies, the growing pediatric obesity epidemic and increasing incidence of type 2 diabetes in children necessitates research aimed at identifying children at risk for developing CVD early in life. Recent adult data have demonstrated that the highest CVD risk amongst pre-diabetes subjects may be in those with IFG. We hypothesize that pediatric patients with IFG have more vascular dysfunction than sex-, race-, and body mass index (BMI)-matched patients with normal glucose metabolism (NGM). Radial artery tonometry and reactive hyperemia peripheral artery tonometry (RH-PAT) are two noninvasive surrogate measurements of arterial stiffness and endothelial function that have been used to predict future CVD in adults and have been used to demonstrate abnormalities in other pediatric populations with elevated CVD risk. We will obtain radial tonometry and RH-PAT measurements in patients 10-18 years of age with IFG. Documentation of increased arterial stiffness and endothelial dysfunction in children with IFG will support aggressive intervention in pediatric populations with IFG to prevent morbidity and mortality associated with CVD.