Defective Energy Metabolism in ME/CFS

About

Status:

Completed

Principal investigator:

Øystein Fluge, Olav Mella, Karl Johan Tronstad

Country:

Norway

Study start:

2017-07

Completion (planned):

2021-02

Last update:

2025-07-20

Research types:

Basic research

Research areas:

Immune system dysfunction, Nutritional and metabolic system dysfunction

Interventions:

Not applicable

Priv. Sector Partner:

Not available

Sponsors:

The Research Council of Norway

Links

Project website

Other website

Project description

The project is one of four projects towards user-identified research on ME/CFS, funded by the Norwegian Research Council. The main objective of this project is to acquire new knowledge of ME/CFS mechanisms to promote the development of new treatment methods and biomarkers. Researchers in Bergen will respond to these needs by investigating whether metabolic disorders are involved in the disease mechanism for this serious and relatively common condition. The project is building upon close cooperation with Professor Olav Mella and Øystein Fluge at the Department of Oncology and Medical Physics at Haukeland University Hospital, which has been receiving support from The Kavli foundation for several years.

The research group of Prof Mella and Fluge has coordinated the collection of samples from over 200 ME/CFS patients and 100 healthy control subjects in a research biobank. This biobank will now be used to study molecular mechanisms in the laboratory. Among other things, changes in the patient's energy metabolism will be mapped by measuring biochemical changes in the patient's blood (metabolomics). At the same time, it will be investigated whether hereditary changes in genes can explain increased disease risk. This is done by means of exome sequencing, comparing genes of sick and healthy family members. This will identify key factors, which will be the starting point for further mechanistic laboratory studies.

The researchers have previously been successful in finding that the function of a metabolic enzyme, pyruvate dehydrogenase, is inhibited in ME/CFS patients. This inhibition probably means that the patient's cells have less energy available, leading to exaustion and fatigue. Based on this finding, the hypothesis is that ME/CFS patients have limitations in the ability to generate energy (adenosine triphosphate or ATP), as well as increased effort-induced production of lactate. Additionally, there are several indications that ME/CFS may be due to a malfunctioning immune response.

Description adapted from project website: see link above.