Karl Tronstad

Karl Johan Tronstad, PhD, is a professor in the Department of Biomedicine, University of Bergen, Bergen, Norway, where he heads the Tronstad Lab which studies cell metabolism and mitochondrial involvement in cancer and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). In 2017, his research group received a grant of 9.5 million for the development of new ME/CFS treatment methods and biomarkers. Dr. Tronstad collaborates with Professor Olav Mella and Øystein Fluge at the Department of Oncology and Medical Physics at Haukeland University Hospital on ME/CFS research.

Notable ME/CFS studies

 * 2016, Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome "Abstract: Myalgic encephalopathy/chronic fatigue syndrome (ME/CFS) is a debilitating disease of unknown etiology, with hallmark symptoms including postexertional malaise and poor recovery. Metabolic dysfunction is a plausible contributing factor. We hypothesized that changes in serum amino acids may disclose specific defects in energy metabolism in ME/CFS. Analysis in 200 ME/CFS patients and 102 healthy individuals showed a specific reduction of amino acids that fuel oxidative metabolism via the TCA cycle, mainly in female ME/CFS patients. Serum 3-methylhistidine, a marker of endogenous protein catabolism, was significantly increased in male patients. The amino acid pattern suggested functional impairment of pyruvate dehydrogenase (PDH), supported by increased mRNA expression of the inhibitory PDH kinases 1, 2, and 4; sirtuin 4; and PPARδ in peripheral blood mononuclear cells from both sexes. Myoblasts grown in presence of serum from patients with severe ME/CFS showed metabolic adaptations, including increased mitochondrial respiration and excessive lactate secretion. The amino acid changes could not be explained by symptom severity, disease duration, age, BMI, or physical activity level among patients. These findings are in agreement with the clinical disease presentation of ME/CFS, with inadequate ATP generation by oxidative phosphorylation and excessive lactate generation upon exertion.

Online presence

 * ResearchGate

Learn more

 * Finding the cause of Chronic Fatigue Syndrome/ME (2017)
 * Tronstad Lab bio page