Fatty liver disease occurs when excess fat accumulates in liver cells and can progress from a silent condition to serious liver damage. It is broadly divided into nonalcoholic fatty liver disease and alcohol associated fatty liver disease, but both share common mechanisms of injury.

The initial stage involves simple steatosis, where fat builds up yet liver function remains relatively normal. Persistent metabolic stress, often driven by obesity, insulin resistance, type 2 diabetes, high triglycerides and unhealthy diet, can trigger inflammation and cellular injury. This stage is known as steatohepatitis. Over time, chronic inflammation promotes scar tissue formation, or fibrosis, which can advance to cirrhosis and increase the risk of liver failure and liver cancer.

At the cellular level, excess free fatty acids and their toxic derivatives induce oxidative stress, mitochondrial dysfunction and endoplasmic reticulum stress. These processes activate inflammatory pathways and fibrogenic cells in the liver. Genetic variants, such as those affecting lipid handling in liver cells, modify susceptibility and disease severity.

Diagnosis typically relies on blood tests, imaging techniques such as ultrasound, elastography and magnetic resonance imaging, and sometimes liver biopsy to assess inflammation and fibrosis. Lifestyle modification, especially weight loss through diet and physical activity, is the cornerstone of treatment and can reduce liver fat and even reverse early fibrosis. Research is actively exploring medications that target insulin resistance, lipid metabolism, inflammation and fibrogenesis, as well as the gut microbiome. Because fatty liver disease is closely linked to systemic metabolic dysfunction, prevention and management focus on improving overall metabolic health rather than the liver in isolation.