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In the liver, it is the type of fatty acid, not the quantity, that determines the extent of the lipotoxic effects. In hepatocytes, the ratio of monounsaturated fatty acids and saturated fatty acids leads to apoptosis and liver damage. There are several potential mechanisms by which the excess fatty acids can cause cell death and damage.
Injury to hepatocyte and bile duct cells lead to accumulation of bile acid inside the liver. This promotes further liver damage. [38] Non-parenchymal cells such as Kupffer cells, collagen-producing stellate cells, and leukocytes (i.e. neutrophil and monocyte) also have a role in the mechanism.
In many cases, propionic acidemia can damage the brain, heart, kidney, liver, cause seizures and delays to normal development such as walking or talking. The accumulation of propionic acid is known to induce differential responses in different organs. The heart and liver are specific targets of the complication.
The Kupffer cells of liver are phagocytic cells that help in the phagocytosis of dead blood cells and bacteria from the blood. [57] The liver is responsible for immunological effects – the mononuclear phagocyte system of the liver contains many immunologically active cells, acting as a 'sieve' for antigens carried to it via the portal system.
Fatty liver disease (FLD), also known as hepatic steatosis and steatotic liver disease (SLD), is a condition where excess fat builds up in the liver. [1] Often there are no or few symptoms. [1] [2] Occasionally there may be tiredness or pain in the upper right side of the abdomen. [1] Complications may include cirrhosis, liver cancer, and ...
In pathology and medicine, lipid peroxidation plays a role in cell damage which has broadly been implicated in the pathogenesis of various diseases and disease states, including ageing, [3] [4] whereas in food science lipid peroxidation is one of many pathways to rancidity. [5]
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No single mechanism leading to steatosis exists; rather, a varied multitude of pathologies disrupt normal lipid movement through the cell and cause accumulation. [7] These mechanisms can be separated based on whether they ultimately cause an oversupply of lipid which can not be removed quickly enough (i.e., too much in), or whether they cause a failure in lipid breakdown (i.e., not enough used).