|
Method of
Action
Methionine is converted to S-adenosyl methionine, which
then serves as a methyl group donor for the synthesis of substances such as
ethanolamine. Ethanolamine is further methylated in the body and converted to
phosphatidylcholine, which is found in lecithin.
Methionine is also converted into homocysteine, which
reconverted back to methionine through the trans-sulfuration pathway.
Homocysteine should not build up in the body; if it does, it is associated with
an increased risk to heart disease and atherosclerosis. The poor conversion of
homocysteine to methionine is caused by vitamin B-6 deficiency in genetically
susceptible individuals.
Methionine is incorporated into proteins. A major route of
its metabolism involves conversion to S-adenosyl methionine (SAM). SAM is a key
intermediate in the transsulfuration pathway, which results in the manufacture
of diverse substances such as taurine and carnitine. SAM is converted to
homocysteine, which can be reconverted to methionine, but adequate levels of
vitamin B-6 are required. A genetic defect has been found which prevents proper
conversion of homocysteine to methionine. This is associated with increased
risk to atherosclerosis (coronary artery disease). This block can be overcome
by administering higher levels of vitamin B-6 and/or betaine, which promote
these sluggish enzymes and facilitate better conversion of homocysteine to
methionine.
Plasma or urinary levels of homocysteine should be zero.
Elevations indicated increased risk to coronary artery disease. |
