Phosphatidylethanolamine N-methyltransferase

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Phosphatidylethanolamine N-methyltransferase

Phosphatidylethanolamine N-methyltransferase (PEMT) is an enzyme that plays a crucial role in the phospholipid metabolism within the liver. It is responsible for the conversion of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) through a series of methylation reactions. This process is essential for maintaining the proper balance of phospholipids in cellular membranes.

Function[edit | edit source]

PEMT catalyzes the methylation of phosphatidylethanolamine to form phosphatidylcholine. This reaction occurs in three steps, with each step adding a methyl group to the ethanolamine moiety of PE. The methyl groups are donated by S-adenosylmethionine (SAM), which is converted to S-adenosylhomocysteine (SAH) in the process. The overall reaction can be summarized as follows:

PE + 3 SAM → PC + 3 SAH

This pathway is particularly important in the liver, where it provides an alternative route for the synthesis of phosphatidylcholine, complementing the CDP-choline pathway.

Location[edit | edit source]

PEMT is predominantly found in the endoplasmic reticulum and the mitochondria-associated membranes of liver cells. Its activity is crucial for the proper functioning of these organelles, as phosphatidylcholine is a major component of their membranes.

Regulation[edit | edit source]

The activity of PEMT is regulated by various factors, including dietary intake of choline, hormonal signals, and the overall metabolic state of the liver. For instance, a diet deficient in choline can upregulate PEMT activity to compensate for the reduced availability of choline-derived phosphatidylcholine.

Clinical Significance[edit | edit source]

Mutations or deficiencies in the PEMT gene can lead to disorders in phospholipid metabolism, which may result in liver diseases such as non-alcoholic fatty liver disease (NAFLD) and hepatic steatosis. Additionally, altered PEMT activity has been implicated in conditions like cardiovascular disease and metabolic syndrome.

See Also[edit | edit source]

References[edit | edit source]

External Links[edit | edit source]

Contributors: Prab R. Tumpati, MD