General pathology · Cell injury, adaptation and death
Fatty change (steatosis) !
- Lesion
Steatosis is the build-up of fat droplets inside cells, mostly in the liver. It is reversible when the cause is removed.
Updated 2026-11-01
What it is
Steatosis is abnormal accumulation of triglycerides in parenchymal cells. It is most common in the liver, which handles fat, but also occurs in heart, muscle and kidney. It arises when fatty acid delivery or synthesis exceeds oxidation and export as lipoproteins. The main causes are metabolic dysfunction (obesity, insulin resistance) and alcohol; others are protein malnutrition, toxins, drugs and hypoxia.
Structure
- Gross: enlarged, soft, yellow, greasy liver.
- H&E: clear round vacuoles in hepatocytes; fat dissolves during routine processing.
- Frozen section stained with Oil Red O or Sudan shows the fat in red or orange.
- Heart: yellow streaks alternating with red muscle (tigered effect) in chronic hypoxia.
Step by step
- Free fatty acids reach the hepatocyte from adipose tissue or diet, or are made from excess carbohydrate.
- Inside the cell they are oxidized in mitochondria or esterified into triglycerides.
- Triglycerides combine with apolipoprotein B to leave as VLDL.
- Excess influx, blocked oxidation or failed export lets triglycerides collect as droplets.
- Droplets fuse and enlarge; the liver becomes big, yellow and greasy.
- If injury continues, inflammation (steatohepatitis) and fibrosis can follow; if it stops, fat clears.
Clinical notes
- Metabolic dysfunction-associated steatotic liver disease is the most common chronic liver disease worldwide and is rising in Latin America with obesity and diabetes.
- Simple steatosis is reversible, but steatohepatitis can progress to cirrhosis and liver cancer.
Test yourself
Think of the answer, then tap the question to see it.
Why does protein malnutrition (kwashiorkor) cause a fatty liver?
Lack of protein limits apolipoprotein synthesis, so triglycerides cannot be exported as VLDL.
How does alcohol favour fatty liver?
Its metabolism raises the NADH/NAD⁺ ratio, which reduces fatty acid oxidation and increases triglyceride synthesis.
Which form of steatosis signals mitochondrial injury?
Microvesicular steatosis, as in Reye syndrome or acute fatty liver of pregnancy.
Related
- Intracellular accumulations: cholesterol, proteins, hyaline, glycogen
- Reversible vs irreversible cell injury: the point of no return
- Alcohol: how it injures the liver, brain, heart and fetus
- Chemical (toxic) cell injury: direct and after metabolism
- Obesity: leptin, adipokines and its consequences
Related conditions
- Metabolic dysfunction-associated steatotic liver disease (MASLD/NAFLD)
- Alcoholic liver disease (biochemistry)
- Metabolic syndrome
- Obesity
- Type 2 diabetes mellitus
- Kwashiorkor
- Reye syndrome
- Acute fatty liver of pregnancy
- Cirrhosis
Elsewhere in DurgiPedia
- Fatty acid β-oxidation
- Ethanol metabolism
- VLDL (very-low-density lipoprotein)
- Lipoprotein metabolism
- Fatty acid synthesis (lipogenesis)
- Liver: lobule, acinus, hepatocytes, sinusoids, Kupffer cells
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Steatotic Liver Disease | Fatty Liver Disease | MedlinePlus (MedlinePlus, US National Library of Medicine, 2024); Alcoholic liver disease: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024).
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Representative model, for educational purposes only.