Professor Karl Johan Tronstad Professor Institute for Biomedicine , Tronstad Lab, Bergen, Norway Prof. Tronstad completed his graduate studies in biochemistry at the University of Bergen (UiB) in 2002. As postdoc at the Haukeland University Hospital, he studied bioactive compounds with the potential to modulate mitochondrial functions in cancer cells. In 2005 he was recruited to the Department of Biomedicine, UiB, where he started his research group to investigate metabolism and mitochondrial physiology. His laboratory seeks to better our understanding of how defective mitochondrial homeostasis may disturb cell physiology, and how this may be involved in mechanisms of cancer and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Karl was involved with the recent paper to come from Bergen - Journal of Clinical Investigation Insight. The Tronstad Lab investigates cell metabolism and mitochondrial biology and we are very fortunate that he can spare time to participate in the Colloquium. Abstract: Cellular energetics in ME/CFS Irregularities in cellular energy metabolism have been linked to many human diseases, including metabolic disorders, mitochondrial diseases, cancer, neurodegeneration and ME/CFS. The possible consequences of cellular energy failure caused by a metabolic defect are context-dependent, and may range from mild cellular stress to cell death. An energydepleted cellular state may theoretically be counteracted by metabolic rewiring, but if this is not sufficient to re-establish the energy level, additional (patho)physiological responses are activated. The consequences may include elements of cellular fatigue, but the mechanisms involved under such conditions are often poorly understood. Recently we found changes in amino acid levels and gene regulation consistent with altered regulation of the central enzyme pyruvate dehydrogenase (PDH) in patients with ME/CFS compared with healthy individuals. Further, the presence of serum from ME/CFS patients changed energy metabolism in healthy human muscle cells in culture. These findings combined with the anticipated role of dysimmunity in ME/CFS, suggest the presence of an immuno-metabolic Page 48 of 56 www.investinme.org Invest in ME research (Charity Nr. 1153730) pathomechanism. We are now investigating potential mechanisms involved, and characterizing contextual consequences of cellular energy failure, with particular focus on the mitochondrial oxidation machinery. Defects in this machinery are likely to cause energy deficiency and excessive lactate production, which are hallmarks of fatigue and post-exertional malaise (PEM). By using a translational research approach, we investigate whether impaired energy metabolism may be linked to ME/CFS symptoms, which could provide support for the development of new biomarkers and treatments. Our research strategy is to build on existing knowledge that has recently emerged concerning metabolic changes in ME/CFS, and to adopt new methods and strategies for studying the mechanisms at the cellular level. This presentation will discuss our current approaches and recent data. Professor Don Staines The National Centre for Neuroimmunology and Emerging Diseases (NCNED), Griffiths University, Australia Professor Staines has been a public health physician at Gold Coast Population Health Unit. He has worked in health services management and public health practice in Australia and overseas. His interests include collaborative health initiatives with other countries as well as cross-disciplinary initiatives within health. Communicable diseases as well as post infectious fatigue syndromes are his main research interests. A keen supporter of the Griffith University Medical School, he enjoys teaching and other opportunities to promote awareness of public health in the medical curriculum. He is now Co-Director at The National Centre for Neuroimmunology and Emerging Diseases (NCNED), Griffiths University in Australia Abstract not available at time of printing.

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