Tomasz Bednarski Assistant Professor

Postdoctoral Fellow, Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, TN, 2022
Ph.D., Laboratory of Molecular Medical Biochemistry, Nencki Institute of Experimental Biology PAS, Warsaw, Poland, 2017
M.Sc., Biotechnology - Interdepartmental Studies, University of Agriculture, Krakow, Poland, 2011

In my Master’s thesis, I investigated the effects of phytase B—an enzyme that catalyzes the reduction of phytate into myo-inositol phosphates—supplementation on baking characteristics and the texture stability of rye bread. Using chromatographic methods, I was able to establish that the supplementation of rye dough with phytase B has a positive effect on phosphorus bioavailability without affecting baking parameters and the texture stability of breads and determined the optimal dosage of the enzyme to use on an industrial scale.

During my PhD studies, I worked on a project investigating the role of long-chain fatty acids (LCFAs) metabolism in different models of left ventricular hypertrophy (LVH). As the outcome of the PhD project, I was able to assess how certain LCFAs affect cardiac function, investigate fatty acid (FA) metabolism in different models of LVH, and determine the differences in metabolic pathways that diverse pathological and physiological LVH. The goal of my postdoctoral project was to identify metabolic determinants that control the transition from simple hepatic steatosis to progressive liver dysfunction, so that these processes can be targeted in the clinic for disease prevention, diagnosis, or treatment. The overall objective of the project was to apply novel in vivo ¹³C MFA and metabolomics profiling to identify liver phenotypes that accelerate the transition from non-alcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). I was able to successfully determine that sarco/endoplasmic reticulum Ca²⁺-ATPase (SERCA) activation has a potential to stop this transition by increasing ω-3 polyunsaturated fatty acids (PUFAs) content, downregulating de novo lipogenesis rate, and normalizing pyruvate cycling in obese mice. These changes led to the alleviation of redox imbalances between liver and peripheral tissues and the mitigation of the inflammatory response in steatotic hepatocytes by activating anti-oxidant response. I have also shown that liver X receptor (LXR) activation, even though it failed to improve NASH phenotype, was able to significantly decrease inflammation, endoplasmic reticulum (ER) stress, and oxidative stress response, as well as improve insulin sensitivity in obese animals. Collectively, my graduate and postdoctoral experience suggests that targeting specific processes of lipid metabolism might prove highly beneficial for cardiac and hepatic function during obesity and diabetes.

Scientifically, I am striving to combine my knowledge of cardiovascular diseases acquired during my graduate studies with my expertise in computational biology gained during my postdoctoral training. I am leading a research program that integrates in vivo and in vitro studies of metabolic diseases with novel stable isotope tracer methods and mass spectrometry-based metabolomics to identify molecular mechanisms of disease pathogenesis.

To accomplish this, I am harnessing the potential of transcriptomics, proteomics, metabolomics, and the emerging field of fluxomics. The broad applicability, innovation, and highly interdisciplinary nature of my research has great potential for funding, publication, commercialization, and patent creation.