Marc Liesa-Roig, Ph.D. is an Assistant Professor in-residence in the Department of Medicine, Division of Endocrinology, David Geffen School of Medicine at UCLA. His laboratory seeks to identify mitochondrial mechanisms adapting and maladapting to metabolic diseases, with the goal to identify novel therapeutic targets. His research on mitochondria is focused in liver, pancreatic beta cells and brown adipose tissue. Dr. Liesa-Roig graduated with honors in Biochemistry at the Universitat de Barcelona (2003). He completed his doctoral studies late 2008 under the supervision of Prof. Antonio Zorzano at the IRB in Barcelona, examining the regulation of mitochondrial dynamics and Mfn2 in skeletal muscle and their role in insulin resistance. He then joined Boston University School Medicine as a post doctoral fellow in 2009, where he became an Instructor in 2013 and an Assistant Professor in 2015. Dr. Liesa-Roig is currently affiliated with the Molecular Biology Institute (MBI), Molecular, Cellular and Integrative Physiology (MCIP) interdepartmental programs and with the Department of Molecular and Medical Pharmacology at UCLA.
UCLAAssistant Professor In-Residence,Endocrinology, Diabetes and HypertensionMember,Molecular Biology Institute
CHS 27-200F, 650 Charles E. Young Dr. Los Angeles, CA 90095
The role of mitochondria in metabolic diseases
Mitochondria are the organelles responsible for our need to breathe, as they use oxygen both to transform nutrients into usable energy and to build essential components constituting our bodies. Indeed, mitochondria are semi-autonomous organelles that contain their own genome, which encodes for 13 proteins essential to consume oxygen. For this reason, mitochondrial DNA mutations that blunt their capacity to consume oxygen are responsible of lethal and severe diseases. Moreover, changes in mitochondrial function are detected in neurodegenerative diseases, as well as in pathologies resulting of an imbalance in energy consumption, energy expenditure and nutrient handling, such as obesity and type 2 diabetes. Furthermore, the reduction in mitochondrial function observed with age is considered a major component driving fitness decline with age. In this context, our overarching research goals are:
1) Define the molecular machinery by which mitochondria can successfully adapt, protect themselves and execute their function in health.
2) Determine when the crosstalk between mitochondria and the redox state contribute to exacerbate metabolic diseases or represent an adaptation preventing their exacerbation.
3) Test whether the manipulation of the molecular machinery modulating and adapting mitochondrial function can be used to treat metabolic diseases.
Measurements of the mitochondrial redox state, dynamics and respiratory capacity
Mitochondrial function determines energetics, signaling and nutrient consumption. In addition, mitochondria are dynamic organelles that move around the cell, fuse to each other and with larger mitochondria splitting into two units. This dynamism not only determines mitochondrial ATP synthesis location and capacity, but it is essential for quality control and removal of damaged units as well. Thus, we use respirometry to determine mitochondrial function and live imaging to visualize mitochondrial dynamics and compartmentalization of the redox state. Approaches include measurements in tissue, intact cells and isolated mitochondria.