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In my MSc thesis, I have 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 metabolism in different models of left ventricular hypertrophy. In my work I was able to demonstrate for the first time that increased stearoyl-CoA desaturase 1 (SCD1) expression, upregulated lipogenesis, and activation of peroxisome proliferator-activated receptor alpha (PPARα)-dependent β-oxidation pathway in cardiac muscle relate to the development of physiological left ventricular hypertrophy and may be one of the adaptive mechanisms to endurance training. On the other hand, I have shown that triacylglycerol accumulation associated with pressure overload-induced, as well as spontaneous hypertension-induced pathological left ventricular hypertrophy is generated by impairment of lipolytic process, and that lack of lipogenesis activation may be one of the mechanisms leading to development of pathological left ventricular hypertrophy, and in consequence, may lead to cardiac dysfunction.

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 metabolic flux analysis and metabolomics profiling to identify liver phenotypes that accelerate the transition from metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic dysfunction-associated steatohepatitis (MASH). 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 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 antioxidant response. I have also shown that liver X receptor (LXR) activation, even though it failed to improve MASH phenotype, was able to significantly decrease inflammation, endoplasmic reticulum stress, and oxidative stress response, as well as improve insulin sensitivity in obese animals.

Research in my laboratory focuses on applying the newly developed technique of simultaneous in vivo multi-organ metabolic flux analysis to investigate the underlying molecular determinants in metabolic disorders pathogenesis. Scientifically, I am striving to combine my knowledge of cardiovascular diseases acquired during my graduate studies with my expertise in hepatic metabolism and 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 metabolic disease pathogenesis. The broad applicability, innovation, and highly interdisciplinary nature of my research has great potential for funding, publication, commercialization, and patent creation.

Teaching

• NUTR 950