Fatty liver disease FLDalso known as hepatic steatosisis a condition where excess fat builds up in the liver. There are two types of fatty liver disease: non-alcoholic fatty liver disease NAFLD and alcoholic liver disease. Often there are no or few symptoms.
Fatty liver can develop into hepatic fibrosis, cirrhosis or liver cancer. These pathologies can also affect non-obese people, who are then at a higher risk. The condition is also associated with other diseases that influence fat metabolism. Fatty liver FL is commonly associated with metabolic syndrome diabeteshypertensionHälsa och viktand dyslipidemiabut can also be due to any one of many causes: [12] [13].
The fatty change represents the intracytoplasmatic accumulation of triglycerides neutral fats. At the beginning, the hepatocytes present small fat vacuoles liposomes around the nucleus microvesicular fatty change. In this stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus.
In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, giving a characteristic signet ring appearance macrovesicular fatty change. These vesicles are well-delineated and optically "empty" because fats dissolve during tissue processing.
Large vacuoles may coalesce and produce fatty cystswhich are irreversible lesions. Macrovesicular steatosis is the most common form and is typically associated with alcoholdiabetes, obesityand corticosteroids. Acute fatty liver of pregnancy and Reye's syndrome are examples of severe liver disease caused by microvesicular fatty change.
Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in energy consumption and its combustion, resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased.
In addition, alcohol use disorder is known to damage mitochondria and other cellular structures, further impairing cellular energy mechanism. On the other hand, non-alcoholic FLD may begin as excess of unmetabolised energy in liver cells.
Hepatic steatosis is considered reversible and to some extent nonprogressive if the underlying cause is reduced or removed. Severe fatty liver is sometimes accompanied by inflammationa situation referred to as steatohepatitis. Progression to alcoholic steatohepatitis ASH or non-alcoholic steatohepatitis NASH depends on the persistence or severity of the inciting cause.
Pathological lesions in both conditions are similar. However, Hälsa och vikt extent of inflammatory response varies widely and does not always correlate with degree of fat accumulation. Steatosis retention of lipid and onset of steatohepatitis may represent successive stages in FLD progression.
Liver disease with extensive inflammation and a high degree of steatosis often progresses to more severe forms of the disease. Liver cell death and inflammatory responses lead to the activation of hepatic stellate cellswhich play a pivotal role in hepatic fibrosis.