Figure 7.
Role of nutrients in hepatic ROS production. High intake of diets rich in fructose or cholesterol promotes hepatic oxidative stress. Fructose metabolism leads to adenosine triphosphate (ATP) depletion and uric acid production, which both trigger reactive oxygen species (ROS) generation in the liver. High fructose consumption can also cause gut dysbiosis, which influences the liver oxidative status. Dietary cholesterol induces mitochondrial dysfunction and further mitochondrial ROS production. In contrast, several micronutrients such as vitamins, polyphenols, carotenoids, some amino acids (glycine, serine), and others have antioxidant properties and may be beneficial in NAFLD. Other abbreviations: ADP, adenosine diphosphate; F1P, fructose-1-phosphate; Nrf2, nuclear factor erythroid-2-related factor 2; GSH, reduced glutathione; FAs, fatty acids; PUFAs, polyunsaturated fatty acids.