For a variety of reasons, lipid—mainly as triacylglycerol—can accumulate in the liver. Extensive accumulation causes fatty liver and is regarded as a pathologic condition. Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide. When accumulation of lipid in the liver becomes chronic, inflammatory and fibrotic changes may develop leading to nonalcoholic steatohepatitis (NASH), which can progress to liver diseases including cirrhosis, hepatocarcinoma, and liver failure.

Fatty livers fall into two main categories. The first type is associated with raised levels of plasma FFA resulting from mobilization of fat from adipose tissue or from the hydro lysis of lipoprotein triacylglycerol by lipoprotein lipase in extrahepatic tissues. The production of VLDL does not keep pace with the increasing influx and esterification of free fatty acids, allowing triacylglycerol to accumulate, which in turn causes a fatty liver. This occurs during starvation and the feeding of high-fat diets. The ability to secrete VLDL may also be impaired (eg, in starvation). In uncontrolled diabetes mellitus, twin lamb disease, and ketosis in cattle fatty infiltration is sufficiently severe to cause visible pallor (fatty appearance) and enlargement of the liver with possible liver dysfunction.

The second type of fatty liver is usually due to a metabolic block in the production of plasma lipoproteins, thus allowing triacylglycerol to accumulate. Theoretically, the lesion may be due to (1) a block in apolipoprotein synthesis (or an increase in its degradation before it can be incorporated into VLDL), (2) a block in the synthesis of the lipoprotein from lipid and apolipoprotein, (3) a failure in provision of phospholipids that are found in lipoproteins, or (4) a failure in the secretory mechanism itself.

One type of fatty liver that has been studied extensively in rats is caused by a deficiency of choline, which has therefore been called a lipotropic factor. Orotic acid also causes fatty liver; it is believed to interfere with glycosylation of VLDL, thus inhibiting release, and may also impair the recruitment of triacylglycerol to the particles. A deficiency of vitamin E enhances the hepatic necrosis of the choline deficiency type of fatty liver. Added vitamin E or a source of selenium has a protective effect by combating lipid peroxidation. In addition to protein deficiency, essential fatty acid and vitamin deficiencies (eg, linoleic acid, pyridoxine, and pantothenic acid) can cause fatty infiltration of the liver.

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مواضيع ذات صلة

Brown Adipose Tissue Promotes Thermogenesis

Hormones Regulate Fat Mobilization

Adipose Tissue is The Main Store of Triacylglycerol in The Body

Classification of Proteins

Precipitation Reactions of Proteins

Study of Protein Structure

The Liver Plays A Central Role in Lipid Transport & Metabolism

HDL Takes Part in Both Lipoprotein Triacylglycerol & Cholesterol Metabolism

Tertiary Structure of Proteins

Secondary Structure of Proteins

Primary Structure of Proteins

Chylomicrons & Very-low Density Lipoproteins are Rapidly Catabolized