Northwestern University

Thu 10:00 AM

BMG Seminar: Understanding how enzyme promiscuity, nutrition, and lipid diversity contribute to cancer and obesity - Christian Metallo, PhD

When: Thursday, October 11, 2018
10:00 AM - 11:00 AM  

Where: Robert H Lurie Medical Research Center, Baldwin Auditorium, 303 E. Superior, Chicago, IL 60611 map it

Audience: Faculty/Staff - Student - Post Docs/Docs - Graduate Students

Contact: Beverly Kirk   312.503.5217

Group: Biochemistry & Molecular Genetics Seminar Series

Category: Lectures & Meetings


The Department of Biochemistry and Molecular Genetics Departmental Seminar Series presents:

Christian Metallo, PhD
Associate Professor, Department of Bioengineering
University of California at San Diego, Jacobs School of Engineering

Metabolism is central to virtually all cellular functions and contributes to a range of diseases. A quantitative understanding of how biochemical pathways are dysregulated in the context of diseases such as cancer and metabolic syndrome is necessary to identify new therapeutic targets. To this end we apply stable isotope tracers, mass spectrometry, and metabolic flux analysis (MFA) to study metabolism in mammalian cells, animal models, and human patients. We are particularly interested in understanding how amino acid and lipid metabolism are coordinated within distinct tissues and in the context of specific disease state. Using metabolomics and lipidomics approaches, we have identified mechanisms through which serine and branched-chain amino acid (BCAA) metabolism contribute to lipid diversity in the context of cancer, diabetes, and associated neuropathy. We have characterized an endogenous, tissue-specific metabolic pathway through which monomethyl branched-chain fatty acid (mmBCFA) are synthesized in mammals. In addition, we have designed specific diets that drive the production of lipids that can mitigate tumor growth. These studies provide mechanistic insights into how enzyme promiscuity and amino acid metabolism can influence lipid diversity, mitochondrial function, and disease progression. These findings also highlight limitations in the use of traditional knockout models to study biological function and disease relevance.

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