Serum folate and homocysteine and the incidence of acute coronary events: the Kuopio Ischaemic Heart Disease Risk Factor Study
Sari VoutilainenJyrki K. VirtanenTiina RissanenGeorg AlfthanJari A. LaukkanenKristiina NyyssönenJaakko MursuVeli-Pekka ValkonenTomi‐Pekka TuomainenGeorge A. KaplanJukka T. Salonen
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Ischaemic heart disease
Hyperhomocysteinemia
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The concentration of circulating total homocysteine is a sensitive marker of inadequate folate and vitamin B12 status. The elevations of plasma homocysteine concentration are associated with an increased risk of vascular disease. The primary goals of this study were to identify plasma homocysteine concentrations in Thai residents and to test for differences in homocysteine levels among sex and age categories. The authors measured plasma total homocysteine concentrations in 3,345 Shinawatra employees (1,133 males, 2,212 females aged between 20-65 years) by using fluorescence polarization immunoassay (FPIA) method. The mean plasma homocysteine concentrations of males and females were 11.495 and 8.547 micromol/L respectively. Plasma homocysteine concentrations were significantly lower in females than in males (p < 0.0001). The age-specific plasma homocysteine levels were lower in females than in males for each group, but the levels of each group was not significantly different both in males and females. When more than 12 micromol/L was used as the cut-off value, it was found that 33.6 per cent of males and 6.69 per cent of females were classified as hyperhomocysteinemia subjects. The authors concluded that the prevalence of hyperhomocysteinemia in Thai males is more common than in females. Further investigation should be done to clarify the association between serum folate, vitamin B12, vitamin B6 concentrations and plasma homocysteine concentration.
Hyperhomocysteinemia
Plasma homocysteine
Fluorescence polarization immunoassay
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Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases,which may be caused by genetic deficiencies in enzymes responsible for remethylation or transsulfuration of homocysteine, nutritional deficiencies in vitamins, or excessive intakes of methionine. Since transsulfuration pathway is the only irreversible pathway in homocysteine metabolism, its key enzyme cystathionine β-synthase is vital in terminal removement of homocysteine. In addition, Studies have observed that enhanced nitrative stress in hyperhomocysteinemic rats could induce cardiovascular injuries, and peroxynitrite stimulation in vitro resulting in decreased bioactivity of cystathionine β-synthase. Therefore, to determine the contribution of nitrative stress to progression of hyperhomocysteinemia, and how it is related to cystathionine β-synthase, we used three groups of rats (Con with normal diet, HHcy with 2.5% methionine diet, HHcy+FeTMPyP with 2.5% methionine diet +FeTMPyP) to observe the effects of nitrative stress ...
Hyperhomocysteinemia
Transsulfuration
Methionine synthase
Homocystinuria
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Hyperhomocysteinemia
Endothelial Dysfunction
Plasma homocysteine
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Hyperhomocysteinemia
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Methionine is the precursor of homocysteine, a sulfur amino acid intermediate in the methylation and transsulfuration pathways. Elevated plasma homocysteine (hyperhomocysteinemia) is associated with occlusive vascular disease. Whether homocysteine per se or a coincident metabolic abnormality causes vascular disease is still an open question. Animals with genetic hyperhomocysteinemia have so far not displayed atheromatous lesions. However, when methionine-rich diets are used to induce hyperhomocysteinemia, vascular pathology is often observed. Such studies have not distinguished the effects of excess dietary methionine from those of hyperhomocysteinemia. We fed apolipoprotein E-deficient mice with experimental diets designed to achieve three conditions: ( i ) high methionine intake with normal blood homocysteine; ( ii ) high methionine intake with B vitamin deficiency and hyperhomocysteinemia; and ( iii ) normal methionine intake with B vitamin deficiency and hyperhomocysteinemia. Mice fed methionine-rich diets had significant atheromatous pathology in the aortic arch even with normal plasma homocysteine levels, whereas mice fed B vitamin-deficient diets developed severe hyperhomocysteinemia without any increase in vascular pathology. Our findings suggest that moderate increases in methionine intake are atherogenic in susceptible mice. Although homocysteine may contribute to the effect of methionine, high plasma homocysteine was not independently atherogenic in this model. Some product of excess methionine metabolism rather than high plasma homocysteine per se may underlie the association of homocysteine with vascular disease.
Hyperhomocysteinemia
Homocystinuria
Transsulfuration
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Hyperhomocysteinemia
Methionine synthase
B vitamins
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Hyperhomocysteinemia
Plasma homocysteine
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Hyperhomocysteinemia
Transsulfuration
Methionine synthase
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Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases,which may be caused by genetic deficiencies in enzymes responsible for remethylation or transsulfuration of homocysteine, nutritional deficiencies in vitamins, or excessive intakes of methionine. Since transsulfuration pathway is the only irreversible pathway in homocysteine metabolism, its key enzyme cystathionine β-synthase is vital in terminal removement of homocysteine. In addition, Studies have observed that enhanced nitrative stress in hyperhomocysteinemic rats could induce cardiovascular injuries, and peroxynitrite stimulation in vitro resulting in decreased bioactivity of cystathionine β-synthase. Therefore, to determine the contribution of nitrative stress to progression of hyperhomocysteinemia, and how it is related to cystathionine β-synthase, we used three groups of rats (Con with normal diet, HHcy with 2.5% methionine diet, HHcy+FeTMPyP with 2.5% methionine diet +FeTMPyP) to observe the effects of nitrative stress on cystathionine β-synthase. Results showed that in diet-induced hyperhomocysteinemic rats, tHcy levels and nitrative stress increased, surprisingly, pretreatment with peroxynitrite scavenger FeTMPyP ameliorated the level of tHcy as well as nitrative stress. Further experiments showed cystathionine β-synthase bioactivity in HHcy rats was less potent than other groups yet described, and the level of cystathionine β-synthase nitration was the most significant,while the entire trends reversed after FeTMPyP pretreatment. In conclusion, these results highlight for the first time that in diet-induced hyperhomocysteinemic rats, cystathionine β-synthase bioactivity reduction is not just a traditional etiologic factor, but rather an outcome of hyperhomocysteinemia, and resulting from the high level of nitrative stress caused by hyperhomocysteinemia, the cystathionine β-synthase nitration plays a mutual role in hyperhomocysteinemia development via causing the metabolic disorder of homocysteine. These findings may shed a novel light on the homocystine-lowering target of hyperhomocysteinemia.
Hyperhomocysteinemia
Methionine synthase
Homocystinuria
Transsulfuration
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