President's Showcase

Riley Hart

Poster Presentation, Ballroom D
Riley Hart 1.jpg

Steve Madden Undergraduate Research Award

NADPH Oxidase (NOX) Lowers ROS Concentrations and Stimulates Adipose Tissue Lipolysis in Humans
Supervising Professor: Dr. Robert Hickner
Riley Hart is a senior from Pensacola, Florida majoring in Exercise Physiology with minors in Child Development and Biology. After she finishes her undergraduate degree, she intend to pursue a career as a physician assistant. Riley have been involved in research under Dr. Hickner’s Lab studying oxidative stress and vascular health since her sophomore year as a UROP student. Research has been an imperative experience for her undergraduate career and an important piece of her personal and professional development. Additionally, research has provided Riley the opportunity to make impactful contributions to projects aimed at addressing pressing medical issues, reflecting her strong desires to help others and advance the medical field.


Cardiovascular disease (CVD) has risen to alarming levels and remains the leading cause of death in the United States. One of the early signs of CVD is elevations in reactive oxygen species (ROS). NADPH oxidase (NOX) is the main source of ROS in blood vessels, and increased NOX activity may impact CVD related factors, such as fat mobilization (lipolysis) and blood flow. PURPOSE: The overall objective of this study was to investigate how NOX-derived ROS production affects blood flow and lipolysis. METHODS: Sixteen sedentary females (age: 21 ± 5 years; body mass index: 22.2 ± 3.8 kg/m2 ; body fat: 31.6 ± 6.8 %) participated in this study. Microdialysis and a hyperinsulinemic-euglycemic were performed where ROS production was measured as H2O2 concentrations, adipose tissue microvascular blood flow (ATMBF) as ethanol outflow/inflow ratio, and lipolysis as glycerol. Apocynin (APO; NOX inhibitor) was infused via microdialysis to determine the contributions of NOX. RESULTS: APO perfusion significantly reduced H2O2 (APO: 0.69 ± 0.27 mM; Control: 1.14 ± 0.51 mM, p = < .0001), decreased ATMBF (APO: 0.79 ± 0.14; Control: 0.68 ± 0.14, p = 0.001) and glycerol (APO: 35.87 ± 18.79 mmol/L; Control: 41.48 ± 23.73 mmol/L, p = 0.0476). No effect of state (basal or clamp) by APO interactions were detected (p = > 0.05). CONCLUSIONS: Reductions in NOX produced ROS are accompanied by decreased blood flow and lipolysis rates that are independent of insulin-regulated pathways. These findings have critical implications as NOX produced ROS may increase the risk of CVD.

Presentation Materials

Project Materials

Project Documents and Links