Fatty liver disease is a condition in which an excessive amount of fat, particularly triglyceride, accumulates inside liver cells. The medical term for fat accumulation in the liver is hepatic steatosis or steatotic liver disease. A small amount of fat can normally be present in the liver, but excessive accumulation can become clinically important because it may be associated with inflammation, cellular injury, fibrosis and, in advanced cases, cirrhosis or liver cancer.
Fatty liver disease is therefore not a single uniform disorder but a description of a pattern of liver fat accumulation with several possible causes. The two broad clinical settings are metabolic dysfunction-associated steatotic liver disease, abbreviated MASLD, and alcohol-associated liver disease, although other causes such as certain medicines, severe nutritional disturbances and rare inherited disorders can also produce hepatic steatosis.
The terminology used for metabolic fatty liver disease has changed in recent years. The term non-alcoholic fatty liver disease, or NAFLD, was widely used historically, whereas metabolic dysfunction-associated steatotic liver disease, or MASLD, is increasingly used to describe steatotic liver disease associated with metabolic risk factors. Within this spectrum, metabolic dysfunction-associated steatotic liver, historically called non-alcoholic fatty liver, involves liver fat with little or no inflammation or liver injury, whereas metabolic dysfunction-associated steatohepatitis, or MASH, previously called non-alcoholic steatohepatitis or NASH, involves steatosis accompanied by inflammation and liver-cell injury. MASH is clinically more consequential because persistent inflammation and injury can stimulate fibrosis, the accumulation of scar tissue.
Fatty liver disease is often described as a silent condition because many people have no noticeable symptoms, particularly during the earlier stages. It may therefore be discovered incidentally when routine blood tests show abnormal liver enzymes or when an abdominal ultrasound, CT scan or other imaging examination performed for another reason shows fat in the liver. The absence of symptoms does not necessarily mean that the liver is completely unaffected, because clinically important fibrosis can develop without prominent warning symptoms. Conversely, the presence of fat on a scan does not automatically mean that advanced liver damage exists. Doctors therefore distinguish the presence of steatosis from the degree of inflammation and fibrosis rather than treating all fatty liver findings as equivalent.
The progression of fatty liver disease varies substantially between individuals. Simple steatosis may remain relatively stable for years and may not produce significant liver injury, whereas MASH can cause persistent inflammation and hepatocyte damage that promotes fibrosis. Fibrosis represents scar formation within the liver and can progress through increasing stages of architectural distortion. Advanced fibrosis can develop into cirrhosis, in which extensive scarring and structural changes impair liver function and blood flow. Cirrhosis can produce complications including portal hypertension, ascites, variceal bleeding, hepatic encephalopathy, liver failure and increased risk of hepatocellular carcinoma. Not everyone with fatty liver develops these complications, and progression is influenced by metabolic, genetic, environmental and liver-specific factors.
Fatty liver disease is closely connected with metabolic health. MASLD is particularly associated with overweight or obesity, increased abdominal adiposity, insulin resistance, type 2 diabetes, high triglycerides, abnormal cholesterol levels, high blood pressure and metabolic syndrome. These conditions can alter the way fatty acids and glucose are processed, increasing the delivery and production of fat within the liver while impairing normal lipid handling.
The liver can become an important site of excess fat storage when energy intake, insulin signalling and lipid metabolism become chronically dysregulated. The relationship is bidirectional: metabolic dysfunction increases the risk of fatty liver, while clinically significant fatty liver can occur as part of a wider pattern of cardiometabolic disease.
Diagnosis involves determining that hepatic steatosis is present and then assessing its likely cause and the extent of liver injury. Medical history is important because clinicians consider alcohol consumption, body weight, diabetes, lipid abnormalities, medicines, nutritional status and other illnesses. Blood tests can assess liver enzymes and other indicators, although normal liver enzymes do not reliably exclude significant liver disease.
Imaging such as ultrasound can demonstrate hepatic fat, while more specialised techniques such as transient elastography can help estimate liver stiffness and therefore the likelihood of significant fibrosis. In selected situations, liver biopsy can provide microscopic information about steatosis, inflammation and fibrosis, although it is invasive and is not necessary for every person with suspected fatty liver disease.
Treatment depends on the cause and severity, but metabolic fatty liver disease is strongly influenced by lifestyle and management of associated metabolic conditions. For people who are overweight, gradual and sustained weight loss can reduce liver fat and may improve inflammation and liver injury; physical activity can improve insulin sensitivity and metabolic health even independently of major weight change.
A balanced diet, appropriate calorie intake, regular exercise, management of diabetes and abnormal blood lipids, and avoidance of excessive alcohol are important components of management. NHS guidance advises people with non-alcoholic fatty liver disease to eat a balanced diet, exercise regularly, aim for at least 150 minutes of activity a week and lose weight if overweight.
Fatty liver disease should not be confused with liver failure, hepatitis or cirrhosis. Steatosis describes excess fat; hepatitis describes inflammation of the liver; fibrosis describes scar formation; and cirrhosis describes advanced architectural scarring and permanent structural damage. These processes can coexist, but they are not synonymous. Fatty liver can also occur because of alcohol rather than metabolic dysfunction, so the presence of hepatic fat does not by itself establish MASLD.
The condition is important because it links liver health with broader metabolic health, including cardiovascular and diabetes-related risk, while its early stages may be reversible or modifiable. Recognising the condition and determining whether fibrosis is present are therefore more informative than simply asking whether fat exists in the liver.
