Non-alcoholic fatty liver disease (NAFLD), the most prevalent liver condition globally, impacts nearly 25% of the world’s population. Characterized by an excessive accumulation of fat in the liver, NAFLD frequently occurs in individuals who are overweight or obese. With the ongoing surge in obesity rates internationally, the incidence of NAFLD is increasing across the board. Recent animal-based research indicates that aerobic exercise could serve as a potential treatment for NAFLD.
A hallmark of non-alcoholic fatty liver disease is the significant accumulation of lipid droplets (LD) within liver cells. Research shows that aerobic exercise, defined as sustained moderate physical activity, assists in metabolizing fats by diminishing the size of these lipid droplets, thereby alleviating the disease’s severity.
The energy requirements triggered by physical activity initiate controlled modifications in the structural and operational interactions between lipid droplets and mitochondria, the cellular components responsible for energy production in metabolism. This interaction is believed to occur in a specialized subset of mitochondria known as peridroplet mitochondria (PDM). Consequently, there’s an increase in lipid oxidation within this distinct group of mitochondria, a mechanism that aids in thwarting the advancement of the disease.
The functional relationship between lipid droplets (LD) and mitochondria plays a crucial role in maintaining the balance of fat metabolism. While exercise has been recognized as beneficial for fatty liver disease, the direct effects of the disease on the interactions between liver lipid droplets and mitochondria were previously unclear.
In animals that engaged in physical activity, there was a noted reduction in the levels of saturated fatty acids within the liver’s mitochondrial membranes. This implies an enhancement in the fluidity of these mitochondrial membranes. Consequently, these findings indicate the involvement of the Mfn-2 protein in adjusting the fatty acid composition of mitochondrial membranes as a response to physical exercise.
The researchers highlight the critical role of mitofusin 2 (Mfn-2), a protein located on the outer membrane of mitochondria, in this mechanism. This protein is key in altering the interactions between lipid droplets and the targeted mitochondrial population.
Given Mfn-2’s role in shaping mitochondrial structure and liver function, therapeutic interventions that adjust the concentration and activity of Mfn-2 may aid in alleviating inflammation and fibrosis associated with this disease.
This study opens up new avenues for monitoring NAFLD’s progression in patients and crafting innovative approaches to halt its onset.
To view the original scientific study click below:
Mitofusin-2 induced by exercise modifies lipid droplet-mitochondria communication, promoting fatty acid oxidation in male mice with NAFLD
