Metabolic fatty liver disease (MASLD): the silent disease that goes hand in hand with insulin resistance

MASLD is the accumulation of fat in the liver associated with at least one cardiometabolic risk factor, such as abdominal obesity, prediabetes or type 2 diabetes, high blood pressure, elevated triglycerides or low HDL cholesterol. The condition can also occur in people with a normal BMI, particularly if they have excess visceral fat or a genetic predisposition.

Insulin resistance plays a central role. When tissues no longer respond effectively to insulin, more fatty acids enter the bloodstream, and the liver produces and stores more fat. In turn, fatty liver can worsen insulin resistance, blood glucose levels and the lipid profile, creating a self-perpetuating metabolic vicious cycle.

In most people, the disease remains at the steatosis stage for a long time. In some patients, however, liver inflammation—known as MASH (metabolic dysfunction-associated steatohepatitis)—may develop, followed by fibrosis and, in advanced cases, cirrhosis. It is not the amount of fat but the degree of fibrosis that is the most important predictor of liver-related complications.

MASLD is often discovered incidentally because it can progress without obvious symptoms. An abdominal ultrasound can identify steatosis, but it may miss mild forms and does not determine the degree of fibrosis with sufficient accuracy. Normal transaminase levels do not rule out the disease or advanced fibrosis either.

The initial assessment may include AST/TGO, ALT/TGP, GGT, a full blood count including platelet count, blood glucose, glycated haemoglobin and a lipid profile. Depending on the circumstances, the doctor may also recommend tests to rule out other causes of liver damage.

A first step in estimating the risk of fibrosis is the FIB-4 score, calculated using age, AST/TGO, ALT/TGP and platelet count. In general, a value below 1.3 indicates a low risk of advanced fibrosis, while a higher value requires medical interpretation and often further investigation. Thresholds vary according to age, and the score should not be interpreted in isolation.

When risk cannot be ruled out through blood tests, liver elastography, such as FibroScan, may be recommended to estimate liver stiffness. A liver biopsy is not routinely necessary and is reserved for situations in which the diagnosis remains unclear or the result would alter treatment.

Treatment aims both to reduce liver damage and to improve metabolic health. For people who are overweight or have obesity, sustained weight loss of at least 5% of their initial body weight may reduce liver fat, 7–10% may improve inflammation, and a reduction of at least 10% offers the greatest chance of improving fibrosis.

There is no single “fatty liver diet,” and detox regimens do not eliminate liver fat. A sustainable eating pattern rich in vegetables, fruit, pulses, whole grains, fish and unsaturated fats is recommended, while limiting sweetened drinks, excess calorie intake and the frequent consumption of ultra-processed foods.

Physical activity can reduce liver fat and improve insulin sensitivity even without substantial weight loss. In general, at least 150 minutes of moderate aerobic activity per week is recommended, together with two to three strength-training sessions and less time spent sitting.

Controlling diabetes, blood pressure, cholesterol, weight and sleep apnoea is equally important. Treatment is individualised, and alcohol consumption should be discussed with the doctor because it may further contribute to the progression of liver damage.