Obesity's rising prevalence in the general population has sparked widespread concern across the world. According to recent epidemiological research, the prevalence of overweight/obesity in humans grew from 28.8% to 38% between 1980 and 2013. Along with rising obesity rates, non-alcoholic fatty liver disease (NAFLD) has been a common diagnosis in clinical settings. NAFLD is defined as fat accumulation in hepatocytes, which is frequently linked with chronic inflammation and metabolic syndrome. Furthermore, it can predispose to non-alcoholic steatohepatitis (NASH) and cirrhosis when other metabolic stresses occur.
Because mitochondria are the primary location of fatty acid oxidation, mitochondrial dysfunction-induced oxidation retardation is postulated as the direct cause of excessive fat storage in the liver. As a result, NAFLD is frequently seen as a mitochondrial illness. NAFLD patients have been found to have abnormal hepatic mitochondrial function. Furthermore, poor mitochondrial activity might result in persistent ROS generation, leading to oxidative stress and mtDNA damage. As a result of increased lipid peroxidation, mitochondrial dysfunction, and reactive oxygen species (ROS) formation, a vicious cycle is displayed. Furthermore, excessive ROS generation causes inflammation by directly activating the host's inflammatory signalling pathways. Furthermore, growing data shows that mitochondrial dysfunction drives NAFLD development.
Scientists from Jimei University and Fujian Aonong Biological Science and Technology Group Co., Ltd in China highlight that all species store energy as fat, and that a high fat diet can lead to excessive fat storage and liver damage, just as it does in humans. In a recent study, the juvenile spotted seabass (Lateolabrax maculatus) were randomly assigned to one of four groups: a standard fat diet with or without supplement hydroxytyrosol (200mg/kg) or a high-fat diet with or without supplement hydroxytyrosol (200mg/kg).
After eight weeks of intervention, the researchers found that the fish given a high fat diet had greater levels of fat deposition in the liver as well as higher levels of oxidative stress. However, when hydroxytyrosol was added to the diet, both of these symptoms improved.
The findings also demonstrated that a high-fat diet was linked to mitochondrial dysfunction, with hydroxytyrosol once again helping to alleviate these negative alterations.
Further research in zebrafish revealed that hydroxytyrosol may benefit the body by activating PINK-1-mediated mitophagy. Mitophagy is a quality control process in mitochondria that eliminates defective and superfluous mitochondria.
This finding supported the reduction of mitophagy by fatty acid therapy and its improvement by hydroxytyrosol administration.
Furthermore, the data revealed similarities between the mitophagy processes in fish and people, since macroautophagy is the most common kind of mitophagy in humans.
As a conclusion, hydroxytyrosol from olives may repair the deleterious effects of a high fat diet on mitochondrial activity and liver health. Supplementing a high fat diet with hydroxytyrosol resulted in considerable increases in indicators of both liver health and mitochondrial function.
