Non alcoholic fatty liver disease (NAFLD) is now one of the most common chronic liver conditions worldwide and is strongly linked to obesity, type 2 diabetes and metabolic syndrome. It ranges from simple fat accumulation in liver cells to non alcoholic steatohepatitis (NASH), where inflammation and cell injury appear and can progress to fibrosis, cirrhosis and liver cancer.

Research shows that insulin resistance is central to the disease. It promotes increased delivery of fatty acids to the liver and enhanced liver fat synthesis, while impairing fat export and oxidation. Excessive intake of fructose and refined carbohydrates further drives liver fat production and uric acid formation, which is associated with oxidative stress and mitochondrial dysfunction. Adipose tissue inflammation, altered secretion of adipokines such as adiponectin and leptin, and changes in gut microbiota also contribute.

Genetic variants, especially in the PNPLA3 and TM6SF2 genes, modify susceptibility and influence the risk of progression from simple steatosis to advanced fibrosis and cancer. However, lifestyle and metabolic factors remain dominant drivers, as shown by the rapid rise in disease prevalence parallel to obesity and diabetes epidemics.

Currently, weight loss through calorie restriction and increased physical activity is the most effective intervention. Even a 5 to 10 percent reduction in body weight lowers liver fat and improves inflammation and fibrosis markers. Drugs targeting insulin resistance, lipid metabolism, oxidative stress and inflammatory pathways are under active investigation, and some agents show promise in reducing liver fat and fibrosis, but no single pharmacologic therapy has yet become standard of care for all patients.