A new study has found that aerobic exercise may effectively treat a common liver disease.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease globally and affects almost one in four people, says Study Finds.  One of the key features of NAFLD is the large concentration of lipid, or fat, droplets that build up within the cells of the liver. Now, researchers in Spain and Chile discovered that aerobic exercise may help treat NAFLD.

“Our findings reveal that aerobic exercise, that is, moderate physical activity over time, helps metabolize the fats because it reduces the size of lipid droplets, and therefore, the severity of the disease,” said Maria Isabel Herández-Alvarez, from the Faculty of Biology at the University of Barcelona. “The energy demands induced by the exercise determine regulated changes in physical and functional relationships between fat droplets and mitochondria, the cell organelles that provide energy for metabolism.”

This interaction may take place among a specific population of mitochondria called peridroplet mitochondria or PDM, says Study Finds.

“As a result, there is a higher oxidation of lipids in this specific population of mitochondria, a process that helps prevent the progress of the disease,” she added.

Herández-Alvarez, one of the authors of the study, noted that “the interaction between the lipid droplets (LD) and the mitochondria is functionally important for the homeostasis of fat metabolism.” She added that while exercise improves fatty liver disease, it has been unknown whether the disease had a direct impact on the interactions between hepatic LDs and mitochondria, says a press release from the University of Barcelona.

The study identified the mitofusin (Mfn-2) protein, a protein located in the external membrane of the mitochondria, as an important regulator in the oxidation of fat.

“Considering the Mfn-2 functions in mitochondrial morphology and in the liver, the therapeutic manipulations of the levels and the activity of Mfn-2 could contribute to the improvement of NAFLD-related inflammation and fibrosis,” said Herández-Alverez. “We found a decrease in the content related to saturated fatty acids in the hepatic mitochondrial membranes in animals that had done physical activity. This suggests that membrane fluidity increases in the mitochondria.

“In the case of the 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 suggest that the Mfn-2 protein takes part in the regulation of the composition of fatty acids of the mitochondrial membranes in response to exercise.”

The study was published in the journal Metabolism.

Researchers say these new findings provide new information for both identifying the progression of NAFLD, and for devising new treatments and ways to prevent the disease from developing.