Metabolic fatty liver disease: what it is, why it happens and what can be done

It is one of those diagnoses that tends to turn up by chance: you have a blood test or an ultrasound for some other reason and you are told you have fat in your liver. It sounds mild, almost incidental, and yet metabolic fatty liver disease is now the most common liver disease in the world and is closely bound up with weight, blood sugar and cardiovascular risk. The good news is that, precisely because of that link, it is one of the few liver conditions you can genuinely do something about. Let's go through what it is, why it happens and what the evidence says, nuances included.

What exactly it is and why the name was changed

In June 2023, an international consensus of the leading hepatology societies (AASLD, EASL and ALEH), with 236 panellists from 56 countries, agreed to change the terminology. What used to be called non-alcoholic fatty liver disease (NAFLD) became metabolic dysfunction-associated steatotic liver disease, or MASLD. And the form with inflammation, previously NASH, became MASH (metabolic steatohepatitis). This is not simply a change of label: the new name describes the real cause far better.

MASLD is diagnosed when there is hepatic steatosis (fat in at least 5% of the liver cells) plus at least one cardiometabolic risk factor (for example excess weight, altered blood sugar, high blood pressure or abnormal cholesterol/triglycerides) and, by definition, in the absence of harmful alcohol intake. That last point matters: it is a different disease from alcohol-related liver disease.

The problem is not the fat in itself, but the fact that it can progress. The spectrum runs from simple steatosis (fat with barely any inflammation) to MASH (fat with inflammation and cell damage), fibrosis (scarring of the tissue), cirrhosis and, in the most advanced cases, liver cancer. Most people stay in the early stages, but a proportion progress, and that is the reason to take it seriously.

Why it happens: the liver as a mirror of metabolism

The most useful way to understand it, according to the 2024 EASL-EASD-EASO guidelines, is this: MASLD is the liver's expression of insulin resistance. When there is a sustained calorie overload and fat accumulated around the internal organs (what is known as visceral obesity), an excess of fatty acids reaches the liver and the liver itself starts producing fat. That build-up of lipids becomes toxic to the liver cells (lipotoxicity) and triggers oxidative stress, inflammation and the activation of cells called stellate cells, which are the ones that produce fibrosis or scarring.

This is why metabolic fatty liver disease almost never travels alone: it is very closely associated with obesity, type 2 diabetes, dyslipidaemia (cholesterol and triglycerides) and hypertension. Seeing it in isolation, as a purely liver problem, means missing the bigger picture. In many ways, it is a sign that the metabolism has been under strain for some time.

How many people have it

Far more than you might think. MASLD is estimated to affect more than 30% of the world's adult population. According to the Global Burden of Disease analysis, in 2021 there were 1,267.9 million prevalent cases worldwide, 24.3% more than in 1990. In other words, it is not only common, it is on the rise, in parallel with the rise in obesity and diabetes.

In at-risk groups the figures shoot up. The guidelines estimate that around 65-70% of people with type 2 diabetes have MASLD, and rates are also very high in people with obesity. This is why current recommendations propose screening for fibrosis (with tools such as the FIB-4 index, calculated from a blood test, and liver elastography, which measures liver stiffness) in people with type 2 diabetes and in obesity with metabolic risk factors. The idea is simple: detect it before there is scarring.

What the evidence says about losing weight

This is where the link with weight stops being theoretical. A classic study (Vilar-Gomez and colleagues, 2015) followed people with biopsies after they lost weight through lifestyle changes and found that the improvement in the liver was dose-dependent: the more weight lost, the better the liver did. With a loss of at least 10% of body weight, 90% had resolution of NASH (what we now call MASH) and 45% showed regression of fibrosis. With a loss of at least 5%, resolution already reached 58%.

Those are powerful figures, but they deserve an honest reading. Losing weight is the best-evidenced intervention, and losing a lot of weight improves the odds. That said, even with large losses (10% or more), fibrosis only regressed in slightly fewer than half of cases. Advanced fibrosis, scarring that is already established, is more stubborn and can persist despite substantial weight loss, including the weight loss achieved with bariatric surgery. Losing weight helps a great deal and is the first thing to be considered, but it is not an automatic guarantee for everyone.

The new medicines: what they do and what they don't yet do

For years it was said that there was no specific medicine for fatty liver. That is no longer true. Resmetirom (a partial thyroid hormone receptor beta agonist) is the first drug to have demonstrated efficacy confirmed by biopsy. In the phase 3 MAESTRO-NASH trial, with 966 patients with MASH and F1B-F3 fibrosis, resolution of MASH without worsening of fibrosis was 25.9% with the 80 mg dose and 29.9% with 100 mg, compared with 9.7% on placebo; and improvement in fibrosis by at least one stage, without worsening of MASH, was 24.2% and 25.9% versus 14.2% on placebo.

Along the same lines, Semaglutide 2.4 mg weekly (a drug from the GLP-1 family, the same one used in obesity and diabetes) produced results in the phase 3 ESSENCE trial, with 800 patients with F2-F3 MASH. At 72 weeks, resolution of steatohepatitis without worsening of fibrosis was 62.9% versus 34.3% on placebo, and improvement in fibrosis without worsening of MASH was 36.8% versus 22.4%. One detail that fits with everything above: the effect correlates with the amount of weight lost. If you want to understand how this family of drugs works, we explain it in detail in our guide on what GLP-1s are.

Now for the essential caveats. None of these medicines makes the disease disappear or works for everyone. Resmetirom is approved only for non-cirrhotic MASH with moderate to advanced fibrosis (F2-F3); the trials did not show benefit in cirrhosis (F4). And there is an underlying limitation that needs saying plainly: the results of these studies are histological improvements, that is, improvements in what is seen on the biopsy. That is an intermediate or surrogate endpoint. A liver that looks better on biopsy is an encouraging sign, but these trials have not yet shown that it translates into fewer deaths, fewer transplants or less liver cancer. It is a real advance, not a finishing line.

The situation in Spain

Resmetirom (brand name Rezdiffra) received a conditional marketing authorisation on 18 August 2025 valid across the whole European Union, and therefore in Spain, for non-cirrhotic MASH with moderate to advanced fibrosis (F2-F3). Since 26 March 2026 it is no longer the only one: semaglutide, under the brand name Kayshild, also holds a conditional authorisation in the EU for that same indication, always alongside diet and exercise. The other GLP-1s remain authorised in Spain for type 2 diabetes and/or obesity, without a specific indication for fatty liver. That said, authorisation is not the same as availability: as things stand it has not been verified whether the Spanish National Health System funds these medicines, at what price, or how readily available they actually are in hospital pharmacies. All of this changes quickly and is worth checking case by case.

Common myths, dismantled

• "Fatty liver is the same as an alcoholic's liver." No. By its very definition, MASLD is diagnosed in the absence of harmful alcohol intake. They are different diseases, even if both end up with fat in the liver.
• "It only happens to people with obesity." False. There is such a thing as lean MASLD, metabolic fatty liver disease in slim people. Weight is a huge risk factor, but not the only one; insulin resistance can be present without obvious obesity.
• "It's just a bit of fat, nothing happens." Not so. Although many people stay in the mild stages, the disease can progress to cirrhosis and liver cancer, and it is also associated with higher cardiovascular risk. Playing it down is precisely the mistake.
• "There is no drug treatment at all." No longer true: since 2024 in the US and since 2025 in the EU there have been medicines authorised for a specific indication: resmetirom and, in the EU since March 2026, semaglutide as well.
• "Losing weight is bound to fix it." Losing weight is what works best and greatly improves the outlook, but regression of fibrosis happens in a minority of cases (around 45% even with large weight losses) and advanced scarring can persist. It is a powerful tool, not a guarantee.

So what can be done

The thread running through all of the above is an encouraging one: metabolic fatty liver disease is not a life sentence. Sustained weight loss is, as things stand, the intervention with the best evidence, and for the first time there are medicines that have been shown to improve the liver in selected patients. But it is also a condition that calls for judgement: which stage you are at, whether or not there is fibrosis, which other metabolic factors you have alongside it and which option fits your case are questions that cannot be answered by an article, only by an individual assessment. If you are interested in how a medical approach to weight loss is put together, we go into it in our guide to the price and the approach of medical treatment in Spain.

If you have been told you have fatty liver, or you have type 2 diabetes, obesity or other metabolic factors, the sensible step is to assess whether screening for fibrosis is worthwhile and to act on the lever with the best evidence: sustained weight loss. What does exist in Spain today is medical weight loss treatment, with a prior assessment, a prescription where appropriate from a registered doctor and ongoing follow-up. If you want to know whether it fits your case, you can check whether you're eligible.