The liver processes nutrients, regulates blood sugar, synthesizes proteins, and manages fats by absorbing and distributing lipids throughout the body. Hepatic steatosis, commonly known as fatty liver, is defined by the excessive accumulation of fat within liver cells (hepatocytes). The condition is confirmed when fat content exceeds 5% of the liver’s overall weight. Hepatic steatosis is very common globally, affecting approximately one-quarter to one-third of the population. Early stages are often asymptomatic, meaning individuals may be unaware they have it until routine medical testing is performed.
The Process of Fat Accumulation in the Liver
Hepatic steatosis begins when fat entering the liver exceeds its capacity to process and export it. This excess fat is stored as triglycerides within hepatocytes. The imbalance stems from increased fatty acid delivery, increased fat synthesis within the liver, or a deficient ability to export triglycerides as very low-density lipoprotein (VLDL).
When fat accumulation is simple and lacks associated injury, it is termed simple steatosis. This stage is often considered reversible if the underlying cause is addressed through appropriate interventions. Simple steatosis indicates a metabolic imbalance.
A more concerning progression occurs when fat accumulation is accompanied by inflammation and damage to liver cells. This advanced stage is known as steatohepatitis, or metabolic dysfunction-associated steatohepatitis (MASH), formerly NASH. Inflammation, cellular ballooning, and hepatocyte death initiate a wound-healing response.
This persistent inflammatory response can activate hepatic stellate cells, which are the primary cells responsible for producing scar tissue. Over time, repeated injury and repair lead to the buildup of scar tissue, known as fibrosis. If fibrosis progresses extensively, it can result in cirrhosis, a severe form of scarring that impairs liver function and increases the risk of liver cancer.
Primary Factors Contributing to Hepatic Steatosis
Hepatic steatosis is broadly categorized into two major types: metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD). The distinction between these types guides management strategies.
MASLD, previously known as non-alcoholic fatty liver disease (NAFLD), is the most common form in industrialized nations and is strongly linked to metabolic syndrome. This condition is defined by hepatic steatosis along with at least one cardiometabolic risk factor, including obesity, Type 2 diabetes, high blood pressure, and dyslipidemia (abnormal cholesterol or triglyceride levels).
Insulin resistance is a central mechanism in MASLD, often occurring in people with excess body weight. When cells become resistant to insulin, the liver is exposed to an increased flow of free fatty acids from dysfunctional adipose tissue. This influx overwhelms the liver’s processing capacity, leading to fat storage.
Alcohol-associated liver disease (ALD) is the other major cause, resulting from chronic, excessive alcohol consumption. Alcohol interferes directly with the body’s ability to break down and remove fats from the liver. This metabolic disruption causes fat to accumulate rapidly within the liver cells.
The progression of ALD depends on the duration and quantity of alcohol consumed, with daily consumption being a particularly strong risk factor. While the pathology of simple steatosis in both MASLD and ALD can look similar under a microscope, their underlying causes are distinct. A third category, MetALD, exists for patients who have both metabolic risk factors and a moderate level of alcohol intake, acknowledging the combined risk.
Clinical Detection and Assessment
Hepatic steatosis is often described as a silent disease because most patients report no symptoms in the early stages. When symptoms do occur, they include fatigue or a dull ache in the upper right side of the abdomen. The condition is frequently discovered incidentally during routine blood work or imaging for unrelated medical issues.
Initial blood tests check for elevated liver enzymes, specifically alanine aminotransferase (ALT) and aspartate aminotransferase (AST). High levels suggest damaged liver cells are leaking their contents into the bloodstream. However, many individuals with fatty liver, even advanced stages, may have entirely normal enzyme levels.
If steatosis is suspected, medical imaging is used to visualize the liver. Standard abdominal ultrasound is a common first step, as it can detect fat accumulation, which makes the liver appear brighter than normal. More detailed imaging, such as a computed tomography (CT) scan or magnetic resonance imaging (MRI), can provide a more precise quantification of the fat content.
To assess disease progression, non-invasive tools check for liver stiffness, a sign of fibrosis. FibroScan (transient elastography) is a specialized ultrasound that measures both liver stiffness and the degree of fat accumulation using the Controlled Attenuation Parameter (CAP). This technology provides numerical values that help doctors monitor disease severity. While these non-invasive methods are widely used, a liver biopsy, involving the removal of a small tissue sample, remains the most definitive way to stage the extent of inflammation and fibrosis.
Pathways for Management and Reversal
Management focuses on halting disease progression and reversing fat accumulation. Lifestyle modification is the most effective intervention and the primary approach for nearly all patients. This includes dietary changes and increased physical activity aimed at sustained weight reduction.
Weight loss is directly associated with improvements in liver health, impacting steatosis, inflammation, and even fibrosis. Losing at least 5% of body weight can improve steatosis. The generally recommended target is a sustained reduction of 7% to 10%. Achieving this higher level of weight loss has been shown to improve or resolve steatohepatitis and, in many cases, decrease the stage of fibrosis.
Dietary changes should prioritize a reduction in overall caloric intake, often through a hypocaloric diet with a daily deficit of 500 to 750 kilocalories. A focus is limiting refined sugars, particularly fructose, and excessive saturated fats, which contribute to fat synthesis in the liver. Diets modeled after the Mediterranean style, rich in vegetables, whole grains, and healthy fats, are frequently recommended for metabolic health.
Physical activity is another important component, even if significant weight loss is not immediately achieved. Moderate-intensity exercise for at least 150 minutes per week has been shown to reduce fat content in the liver. Both aerobic exercise and resistance training contribute to improved insulin sensitivity, which helps the liver better regulate fat metabolism. Combining dietary changes with exercise yields a greater reduction in liver fat deposits than either intervention alone.
In addition to lifestyle adjustments, managing underlying metabolic conditions is necessary. This involves carefully controlling Type 2 diabetes, hypertension, and high cholesterol through medication and lifestyle changes. For patients with confirmed MASH and advanced fibrosis, certain pharmacological treatments may be considered.
Some drugs, such as Pioglitazone, can improve liver histology, and Vitamin E may be used in non-diabetic patients with MASH. Specific medications like Resmetirom have recently been approved for use in patients with MASH and significant liver scarring, though they are not indicated for those who have progressed to cirrhosis. A multidisciplinary approach emphasizing sustainable lifestyle modification remains the most reliable pathway for managing and potentially reversing hepatic steatosis.