Role of Oxidative Stress in Hepatic and Extrahepatic Dysfunctions during Nonalcoholic Fatty Liver Disease (NAFLD)

Figure 1

Intrahepatic complications in nonalcoholic fatty liver disease (NAFLD). NAFLD’s pathophysiology is affected by genetic and environmental factors such as diet, bisphenol A (BPA), leading to obesity and insulin resistance (IR). Adipose tissue gain contributes to chronic low-grade inflammation and increases free fatty acids (FFA) mobilization, resulting in visceral and ectopic fat deposition. In NAFLD, one of the main alterations is the hepatic steatosis. Thus, steatosis increases FFA, which increases intrahepatic triglycerides levels. This significant lipidic increase inside the liver results in lipotoxicity and oxidative stress (OS). OS and lipotoxicity induce mitochondrial dysfunction, hepatocyte apoptosis, and hepatic inflammation, increasing profibrotic factors that contribute to liver fibrosis. Besides, there is a failed attempt to regenerate the liver. Together, these tissue alterations contribute to hepatic dysfunction. Together, the impaired lipidic metabolism, the increase of proinflammatory cytokines, and the OS can induce hepatic dysfunction that favors NAFLD progression. Created with http://BioRender.com.