The most common liver disease on the planet, the non-alcoholic fatty liver disease (Nafld), also known as “non-alcoholic fatty liver”, affects almost one in four individuals globally. This accumulation of fat in the liver is common among overweight or obese patients. And as obesity rates continue to increase around the world, more and more people around the world are developing Nafld. A new study, based on experiments on mice and published in the journal Metabolismdiscovered that theaerobic exercise can help treat precisely this type of pathology.
One of the main characteristics of non-alcoholic fatty liver disease is in fact the large concentration of lipid droplets (LD) that accumulate inside the liver cells. «Our results reveal that aerobic exercise, i.e moderate physical activity over timehelps metabolize fats because it reduces the size of lipid droplets and therefore the severity of the disease” he explains María Isabel Herandez-Alvarezprofessor at the Faculty of Biology at the University of Barcelona, at the Institute of Biomedicine and at the Biomedical Research Network Center on Diabetes and Associated Metabolic Diseases.
«Therefore, the energy demands induced by exercise determine regulated changes in physical and functional relationships between fat droplets and mitochondria, the cellular organelles that provide energy for metabolism” adds Herández-Alvarez. This interaction can occur between a specific population of mitochondria called mitochondria peridroplet. “As a result, increased lipid oxidation occurs in this specific population of mitochondria, a process that helps prevent the disease from progressing.” The authors of the study highlight in particular that the mitofusin 2 (Mfn-2), a protein present in the outer membrane of the mitochondria, appears to play a decisive role in this beneficial process triggered by exercise. The protein actually modifies the communications between the lipid droplets and the specific mitochondrial population.
«We found a decrease in the content of saturated fatty acids in the hepatic mitochondrial membranes of animals that had performed physical activity. This suggests that membrane fluidity increases in the mitochondria,” explains the scientist. «In the case of mice without the Mfn-2 gene, exposed to physical activity, we did not observe changes in the saturation and metabolism of fatty acids. These results show that the Mfn-2 protein participates in the regulation of the fatty acid composition of mitochondrial membranes in response to physical exercise.”
