Dr. Jurczak’s lab is primarily interested in the relationship between nutrient excess, mitochondrial overload and the pathogenesis of metabolic diseases, such as fatty liver, insulin resistance and type 2 diabetes. Mitochondrial dysfunction and ectopic lipid accumulation in liver are both associated with insulin resistance in human subjects, but the cause and effect nature of these associations remain unclear. Dr. Jurczak’s lab is specifically interested in a mitochondrial repair mechanism called mitophagy that regulates the selective removal of damaged mitochondria via the autophagosomal pathway. Because autophagy is suppressed in mouse models of obesity and fatty liver disease, it is likely that mitophagy is similarly impaired and may contribute to the decline in mitochondrial function seen in human patients. Interestingly, a key component of the mitophagy pathway, a ubiquitin E3 ligase called Parkin, is upregulated in liver of obese mice. This change may represent a compensatory response to remove damaged mitochondria from hepatocytes or result directly from the loss of autophagy. Dr. Jurczak’s group is using a genetic approach to test whether the loss of Parkin-mediated mitophagy in liver predisposes mice to mitochondrial dysfunction, ectopic lipid accumulation and insulin resistance. The lab employs in vivo and ex vivo approaches in transgenic mouse models and specializes in using radioactive and stable metabolic isotopes to measure substrate turnover and flux.
Dr. Jurczak is involved in mentoring postdoctoral fellows and clinical research fellows in the Department of Medicine, Division of Endocrinology and Metabolism.
- BS, University of California Los Angeles, 2002
- PhD, University of Chicago, 2008
- Post-Doctoral Fellow, Howard Hughes Medical Institute, Yale University, 2011
Education & Training
Xie, B, Ramirez, W, Mills, AM, Huckestein, BR, Anderson, M, Pangburn, MM, Lang, EY, Mullet, SJ, Chuan, BW, Guo, L, Sipula, I, O'Donnell, CP, Wendell, SG, Scott, I, Jurczak, MJ. Empagliflozin restores cardiac metabolic flexibility in diet-induced obese C57BL6/J mice. Current Research in Physiology. 2022; 5: 232-239.
Edmunds, LR, Xie, B, Mills, AM, Huckestein, BR, Undamatla, R, Murali, A, Pangburn, MM, Martin, J, Kaufman, BA, Scott, I, Jurczak, MJ. Liver-specific Prkn knockout mice are more susceptible to diet-induced hepatic steatosis and insulin resistance. Molecular Metabolism. 2020; 41: 101051.
Edmunds, LR, Huckestein, BR, Kahn, M, Zhang, D, Chu, Y, Zhang, Y, Wendell, SG, Shulman, GI, Jurczak, MJ. Hepatic insulin sensitivity is improved in high-fat diet-fed Park2 knockout mice in association with increased hepatic AMPK activation and reduced steatosis. Physiological Reports. 2019; 7(21): e14281.
Thapa, D., Wu, K., Stoner, M. W., Xie, B., Zhang, M., Manning, J. R., Lu, Z., Li, J. H., Chen, Y., Gucek, M., Playford, M. P., Mehta, N. N., Harmon, D., O'Doherty, R. M., Jurczak, M. J., Sack, M. N., Scott, I. The protein acetylase GCN5L1 modulates hepatic fatty acid oxidation activity via acetylation of the mitochondrial ß-oxidation enzyme HADHA. J Biol Chem. 2018; Epub ahead of print.
Jurczak, M. J., Saini, S., Ioja, S., Costa, D. K., Udeh, N., Zhao, X., Whaley, J. M., Kibbey, R. G. SGLT2 knockout prevents hyperglycemia and is associated with reduced pancreatic ß-cell death in genetically obese mice. Islets. 2018; 1-9.
Thapa, D., Stoner, M. W., Zhang, M., Xie, B., Manning, J. R., Guimaraes, D., Shiva, S., Jurczak, M. J., Scott, I. Adropin regulates pyruvate dehydrogenase in cardiac cells via a novel GPCR-MAPK-PDK4 signaling pathway. Redox Biol. 2018; 18: 25-32.
Flannery, C. A., Choe, G. H., Fleming, A. G., Cooke, K. M., Radford, C. C., Kodaman, P. H., Jurczak, M. J., Kibbey, R. G., Taylor, H. S. Insulin Regulates Glycogen Synthesis in Human Endometrial Glands through Increased GYS2. J Clin Endocrinol Metab. 2018; Epub ahead of print.
Xiong, J., Kawagishi, H., Yan, Y., Liu, J., Wells, Q. S., Edmunds, L. R., Fergusson, M. M., Yu, Z. X., Rovira, I. I., Birttain, E. L., Wolfgang, M. J., Jurczak, M. J., Fessel, J. P., Finkel, T. A Metabolic Basis for Endothelial-to-Mesenchymal Transition. Mol Cell. 2018; 69(4): 689-698.e7.
Lawan, A., Min, K., Zhang, L., Canfran-Duque, A., Jurczak, M. J., Camporez, J. P. G., Nie, Y., Gavin, T. P., Shulman, G. I., Hernandez-Fernando, C., Bennet, A. M. Skeletal Muscle-Specific Deletion of MKP-1 Reveals a p38 MAPK/JNK/Akt Signaling Node that Regulates Obesity-Induced Insulin Resistance. Diabetes. 2018; 67(4): 624-635.
Petersen, MC, Jurczak, MJ. CrossTalk opposing view: Intramyocellular ceramide accumulation do not modulate insulin resistance. The Journal of Physiology. 2016; 594(12): 3171-4.
- Committee Award for Outstanding Performance in the General Field of Molecular Metabolism and Nutrition, University of Chicago, 2008
- Inaugural Invited Lecture, Committee on Molecular Metabolism and Nutrition Alumni Lecture, University of Chicago, 2011
- Former Co-Director of the NIH-funded Yale Mouse Metabolic Phenotyping Center In Vivo Metabolism Core, 2011-2015
- American Diabetes Association Research Grant Review Committee Member, 2016
- UPP Academic Foundation Young Investigator Award, University of Pittsburgh School of Medicine, 2016
- Allen Humphrey Excellence in Mentoring Award, University of Pittsburgh School of Medicine, 2017
- Department of Medicine PhD Leadership Council, University of Pittsburgh School of Medicine, 2021-2022
- Medical Student Mentoring Merit Award, University of Pittsburgh School of Medicine, 2022
