President's Showcase

Connor Krassel

Poster Presentation, Ballroom D
Connor Krassel 1.jpg

Helen Louise Lee Undergraduate Research Award

NADPH Oxidase (NOX) Lowers ROS Concentrations and Stimulates Adipose Tissue Lipolysis in Humans
Supervising Professor: Dr. Robert Hickner
Connor Krassel was born in Melbourne, Florida and is currently a Junior Biological Sciences major. He plans on applying to medical school at the end of his undergraduate years with the goal of studying anesthesiology. He has been working as a research assistant in Dr. Hickner’s lab for over a year in the College of Health and Human sciences and is now excited to share his own research with Riley Hart through the IDEA Grant program.


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.

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