Mitochondria are high performing cellular components that are the site of several life-sustaining reactions, including the conversion of food into fuel for the cell. Mitochondria are found in abundance in the liver (about 1000-2000 per cell), which is no surprise. Liver cells have a massive amount of work to do – including metabolism, detoxification, and hormone release – and all that work requires lots of energy.
It is well known that obesity increases the risk of nonalcoholic fatty liver disease (NAFLD). NAFLD is progressive, initially symptomless disease, where deposits of fat in the liver contribute more than 5-10% to the liver’s weight. Satapati and colleagues, in their article published in the Journal of Clinical Investigation, investigated the influence obesity-caused NAFLD had on mitochondria and particularly free radical production.
They found that moderate obesity and NAFLD caused mitochondria to act in a hyperactive, but inefficient way, causing excessive production of free radicals, particularly reactive oxygen species (ROS), leading to oxidative stress and inflammation. This in turn affected the response to insulin and increased the development of diabetes. Unfortunately, more severe obesity-related NAFLD increased the risk of mitochondrial death and further accelerated disease progression.