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Fasting, postprandial, and post‐methionine‐load homocysteinaemia and methylenetetrahydrofolate reductase polymorphism in vascular disease
Author(s) -
Candito M.,
Bedoucha P.,
Gibelin P.,
Jambou D.,
Franchis R.,
Sadoul J.L.,
Chatel M.,
Van Obberghen E.
Publication year - 1999
Publication title -
journal of inherited metabolic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 102
eISSN - 1573-2665
pISSN - 0141-8955
DOI - 10.1023/a:1005513626542
Subject(s) - methylenetetrahydrofolate reductase , postprandial , homocysteine , medicine , vascular disease , methionine , endocrinology , metabolic disease , biology , genetics , genotype , gene , amino acid , diabetes mellitus
Hyperhomocysteinaemia is an independent risk factor for cardiovascular disease. The C677T mutation of the methylenetetrahydrofolate reductase (MTHFR) is a common genetic cause of increased homocysteine (HCY) levels. Post‐methionine‐load HCY concentrations allow identification of certain cases of hyperhomocysteinaemia not demonstrated by fasting levels. This study investigated the relationship between MTHFR polymorphism and (1) fasting HCY levels (77 patients); (2) post‐methionine HCY levels (54 patients); and (3) postprandial HCY concentrations (36 patients) in cardiovascular disease. As expected, mean fasting HCY value was higher in the +/+ patients. Moreover, patients who were homozygous for the mutation exhibited significantly increased mean post‐methionine‐load HCY; in contrast, literature results are conflicting. Mean postprandial HCY, which is not known to be increased in controls, was also increased in the (+/+) patients, although the difference did not reach statistical significance, probably owing to the small size of the sample. MTFHR polymorphism is known to be aggravated by a drop in circulating folate. Additional risk factors may be more prevalent in patients with cardiovascular disease.