Homocysteine and Cardiovascular Disease

Barter, Philip J.; Rye, Kerry‐Anne

doi:10.1161/01.res.0000243583.39694.1f

Cited by 33 publications

(27 citation statements)

References 24 publications

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“…Hcy has taken a place among other major risk factors of CVD such as cholesterol, smoking, and obesity. However, it is now widely accepted as a major independent risk factor for cardiovascular, cerebrovascular, and peripheral vascular diseases [20]. In this current study, it was found that the hcy level was significantly higher in subjects with PCOS than in control subjects.…”

Section: Discussionsupporting

confidence: 54%

Methylenetetrahydrofolate reductase C677T gene polymorphism in turkish patients with polycystic ovary syndrome

Karadeniz

Erdoğan

Zengi

et al. 2010

Endocr

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Higher Levels of Hcy are associated with several clinical conditions, among them non-insulin-dependent diabetes mellitus, endometrial dysplasia and hypertension with insulin resistance, and polycystic ovary syndrome. The purpose of this study was to investigate the serum homocystein levels and other metabolic parameters in relationship with the MTHFR C677T gene polymorphism in patients with PCOS. Our study included 86 young women with PCOS constituting the study group and 70 healthy women constituting the control group. Homocystein levels, metabolic, and hormonal parameters were measured, and genetic analysis of the MTHFR C677T gene polymorphism was performed in all the subjects. A statistically significant difference was observed in mean homocystein levels between patients with PCOS when compared to the control group. The MTHFR 677 CC genotypes had significantly higher proportions in the control group compared to the PCOS patients (χ(2) = 21.381, P < 0.001). Our data show that homocystein levels were higher than normal subjects in patients with PCOS and that the MTHFR C677T gene polymorphism does not influence homocystein levels of patients with PCOS.

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Section: Discussionsupporting

confidence: 54%

Methylenetetrahydrofolate reductase C677T gene polymorphism in turkish patients with polycystic ovary syndrome

Karadeniz

Erdoğan

Zengi

et al. 2010

Endocr

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“…These studies support the hypothesis that Hcy reduces the concentration of plasma HDL-C and apoA-I in humans and in mice and contributes to accelerated CVD. As pointed out by Barter and colleagues, these findings may explain the results of the FIELD study in which an increase in Hcy during treatment with fenofibrate was associated with a much less than expected increase in HDL-C and a disappointing reduction in cardiovascular events (50,51).…”

Section: Hyperhomocysteinemia and High-density Lipoproteinmentioning

confidence: 82%

Hyperhomocysteinemia and high-density lipoprotein metabolism in cardiovascular disease

Liao¹,

Yang²,

Wang³

2007

Clinical Chemical Laboratory Medicine

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Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular disease (CVD) and the underlying mechanism is unclear. We and others have reported that homocysteine (Hcy) is inversely correlated with plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein AI (apoA-I) in patients with coronary heart disease (CHD). We confirmed this negative correlation in mice with targeted deletions of the genes for apolipoprotein E (apoE) and cystathionine beta-synthase (CBS). Severe HHcy (plasma Hcy 210 micromol/L) accelerates spontaneous arthrosclerosis in the CBS(-/-)/apoE(-/-) mice, reduces the concentration of circulating HDL, apoA-I, and large HDL particles, inhibits HDL function, and enhances HDL-C clearance. We have demonstrated further that Hcy (0.5-2 mmol/L) reduces apoA-I protein synthesis and secretion, but not RNA transcription in mouse primary hepatocytes. A different mechanism was proposed based on studies using the HepG2 cells showing that Hcy (5-10 mmol/L) inhibits apoA-I transcription via peroxisome proliferator-activated receptor-alpha (PPARalpha)-inhibition-dependent and -independent mechanisms. These studies suggest that Hcy-induced HDL-C and apoA-I inhibition represent a novel mechanism by which Hcy induces atherosclerotic CVD.

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“…HHcy might also increase the risk of CVD in dyslipidemia patients [4–6]. Although the mechanism of the link is not thoroughly known, recent studies strongly demonstrated the importance of the metabolic balance between S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), phosphatidylcholine (PC), phosphatidylethanolamine (PE) and choline in Hcy metabolism, hypolipoproteinemia, liver function, and CVD [3, 7]. Several studies relating HHcy to disturbed HDL-C metabolism showed that Hcy can reduce circulating HDL-C via inhibiting ApoA-I protein synthesis and enhance HDL-C clearance [8, 9].…”

Section: Introductionmentioning

confidence: 99%

Relationship between plasma homocysteine level and lipid profiles in a community-based Chinese population

et al. 2017

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BackgroundPrevious studies established a possible link among hyperhomocysteinemia (HHcy), dyslipidemia, and atherosclerosis. However, there was limited epidemic data concerning the relation between HHcy and lipid profiles, especially in community-based Chinese populations. This study aim to investigate the association of plasma homocysteine (Hcy) level with lipid profiles in a Chinese community-based population without lipid-lowering treatment.MethodA total of 4660 Chinese subjects from a cohort of the Shijingshan district in Beijing were included in the analysis. Plasma total Hcy, serum lipid files including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) as well as relevant metabolic risk factors were measured. Multivariate regression models adjusting for age, gender, smoking, drinking, physical activity, vitamin B supplement, body mass index, fasting blood glucose level, serum creatinine, systolic and diastolic blood pressure were used to evaluate associations of Hcy and lipid profiles.ResultSubjects were 56.75 ± 8.91 years old, and 38.15% were male. Median (IQR) Hcy was 11.98 (10.00–14.93) μmol/L, and 24.4% had HHcy (defined as Hcy ≥ 15 μmol/L). Mean (SD) baseline TC was 5.34 ± 0.98 mmol/L, LDL-C was 3.27 ± 0.81 mmol/L, and HDL-C was 1.43 ± 0.38 mmol/L. Median (IQR) of TG was 1.28 (0.91–1.85) mmol/L. In multivariable linear-regression analyses, lnHcy (ln transformation for Hcy) level was positively associated with lnTG (adjusted β = 0.075, SE = 0.021, P = 0.001). Using Hcy < 15 μmol/L as a reference, HHcy was independently associated with both lnTG (adjusted β = 0.056, SE = 0.020, P = 0.004) and lnHDL (adjusted β = −0.018, SE = 0.009, P = 0.038). In multivariable logistic-regression analyses, HHcy was associated with increasing risk of low HDL-C (HDL-C < 1.04 mmol/L; adjusted odds ratio [OR] =1.406, 95% confidence interval [CI]: 1.143 – 1.728, P = 0.001) and hypertriglyceridemia (TG ≥ 1.7 mmol/L; adjusted OR = 1.293, 95% CI: 1.096–1.524, P = 0.002) after adjusting the confounders. However, there were no significant associations between Hcy and TC or LDL-C.ConclusionThe present study showed that HHcy was independently associated with hypertriglyceridemia and low levels of HDL-C, which provides evidence that Hcy levels might affect HDL-C and TG metabolism.

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Homocysteine and Cardiovascular Disease

Cited by 33 publications

References 24 publications

Methylenetetrahydrofolate reductase C677T gene polymorphism in turkish patients with polycystic ovary syndrome

Methylenetetrahydrofolate reductase C677T gene polymorphism in turkish patients with polycystic ovary syndrome

Hyperhomocysteinemia and high-density lipoprotein metabolism in cardiovascular disease

Relationship between plasma homocysteine level and lipid profiles in a community-based Chinese population

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