Hepatic steatosis and liver injury are major health issues linked to obesity and insulin resistance. Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum from simple fatty liver to severe steatohepatitis, which can lead to cirrhosis and liver failure. Insulin resistance is a key driver of NAFLD, increasing triglyceride accumulation in the liver. Recent research highlights molecular mechanisms, including the roles of SREBP-1c, ChREBP, and PPAR-γ in lipid metabolism and fatty acid synthesis. These factors contribute to the development of hepatic steatosis by enhancing lipogenesis and reducing fatty acid oxidation. AMPK activation also plays a critical role in reducing lipogenesis and increasing fatty acid oxidation. Oxidative stress and lipid peroxidation are significant contributors to liver injury in NAFLD, leading to inflammation, fibrosis, and cell death. Mitochondrial dysfunction exacerbates these processes by increasing ROS production and impairing fatty acid metabolism. The two-hit model explains how initial lipid accumulation leads to progressive liver damage through inflammation and fibrosis. Despite advances in understanding these mechanisms, the relationship between hepatic steatosis and nonalcoholic steatohepatitis (NASH) remains unclear. Further research is needed to clarify the progression of NAFLD and develop targeted therapies.Hepatic steatosis and liver injury are major health issues linked to obesity and insulin resistance. Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum from simple fatty liver to severe steatohepatitis, which can lead to cirrhosis and liver failure. Insulin resistance is a key driver of NAFLD, increasing triglyceride accumulation in the liver. Recent research highlights molecular mechanisms, including the roles of SREBP-1c, ChREBP, and PPAR-γ in lipid metabolism and fatty acid synthesis. These factors contribute to the development of hepatic steatosis by enhancing lipogenesis and reducing fatty acid oxidation. AMPK activation also plays a critical role in reducing lipogenesis and increasing fatty acid oxidation. Oxidative stress and lipid peroxidation are significant contributors to liver injury in NAFLD, leading to inflammation, fibrosis, and cell death. Mitochondrial dysfunction exacerbates these processes by increasing ROS production and impairing fatty acid metabolism. The two-hit model explains how initial lipid accumulation leads to progressive liver damage through inflammation and fibrosis. Despite advances in understanding these mechanisms, the relationship between hepatic steatosis and nonalcoholic steatohepatitis (NASH) remains unclear. Further research is needed to clarify the progression of NAFLD and develop targeted therapies.