About Dr. Nicholas

 

     My life’s goal is to advance the current standard of care for type 2 diabetes patients through basic science research. The pervasiveness of type 2 diabetes in my family fuels my drive, determination, and persistence to discovering what mechanisms underlie the etiology of the disease. My dissertation work at Loma Linda University, under the guidance of Drs. De Leon and Langridge, cultivated my interest in how obesity and overnutrition, particularly saturated fat from both adipose tissue and diet, stimulate chronic inflammation that drives insulin resistance and resulting metabolic disease. We found that saturated fatty acids, when present in high enough concentrations, can directly activate immune cell subsets. This activation results in responses such as pro-inflammatory cytokine production and antigen specific antibody responses. These findings are the crux of my first major research question: How and why does the human immune system generate an antigen specific response to saturated fatty acids?

     My first post-doctoral fellowship at Boston University with Dr. Nikolajczyk piqued my interest in alternative mechanisms by which fatty acids impact immune cells, namely cell metabolism. We have so far found that immune cells from people with type 2 diabetes have an impaired ability to utilize fatty acids as fuel. We are currently investigating how defective lipid metabolism in type 2 diabetes may contribute to the accompanying chronic inflammation. This current project has generated my second major research question: How does chronic exposure to increased lipids and glucose (as seen in obesity and overnutrition) impact immune cell function?

     My second post-doctoral fellowship at UCSD under the mentorship of Drs. Mellon and Lawson will allow me to study whole animal physiology, and therefore effectively evaluate the impact of fatty acids on chronic inflammation associated with polycystic ovarian syndrome. My complimentary training in immunology, biochemistry, and now physiology will support my overall research goals of understanding the causal link between obesity/overnutrition and metabolic disease. I am determined to integrate my developing knowledge of basic science research, high dimensional data analysis, mathematical modeling, and whole animal physiology to expand the understudied field of lipid immunology. It is my goal to advance knowledge in this naïve field by challenging the protein-centric dogma currently viewed in immunology to ascertain the role of diet-induced inflammation in the expanding diabetes epidemic.