Plasma homocysteine concentration related to diet, endothelial function and mononuclear cell gene expression among male hyperlipidaemic smokers

Brude, Ingeborg R.; Finstad, Hanne S.; Seljeflot, Ingebjørg; Drevon, Christian A.; Solvoll, Kari; Sandstad, Berit; Hjermann, Ingvar; Arnesen, Harald; Nenseter, Marit S.

doi:10.1046/j.1365-2362.1999.00419.x

Cited by 53 publications

(40 citation statements)

References 61 publications

(80 reference statements)

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“…Three previous studies concerning vWf and tHcy showed a positive correlation in subjects with peripheral arterial occlusive disease [7±9]. In contrast, a study in hyperlipidaemic male smokers showed a signi®cant negative correlation between tHcy and vWf [37]. A recent study performed by de Roo et al demonstrated a weak positive relation between tHcy and the endothelial proteins vWf and endothelin in healthy ) associated with a Model b ln tHcy (95% C.I.)…”

Section: Discussionmentioning

confidence: 92%

Serum homocysteine is weakly associated with von Willebrand factor and soluble vascular cell adhesion molecule 1, but not with C‐reactive protein in type 2 diabetic and non‐diabetic subjects — The Hoorn Study

Becker

Hinsbergh

Kostense

et al. 2000

Eur J Clin Investigation

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Background Hyperhomocysteinaemia may constitute an independent risk factor for cardiovascular disease, but it is still unclear by which pathophysiological mechanisms homocysteine (tHcy) may promote atherothrombosis. The aim of this study was ®rstly to examine whether tHcy is associated with endothelial dysfunction, increased adherence of leukocytes, and/or chronic low-grade in¯ammation, as estimated from plasma levels of von Willebrand factor (vWf), soluble vascular cell adhesion molecule 1 (sVCAM-1) and C-reactive protein (CRP), respectively. Secondly we investigated whether the presence of type 2 diabetes modi®es these associations.

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Section: Discussionmentioning

confidence: 92%

Serum homocysteine is weakly associated with von Willebrand factor and soluble vascular cell adhesion molecule 1, but not with C‐reactive protein in type 2 diabetic and non‐diabetic subjects — The Hoorn Study

Becker

Hinsbergh

Kostense

et al. 2000

Eur J Clin Investigation

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“…Homocysteine (Hcy) may play an important role in the atherothrombogenic process [3][4][5][6]. The beneficial actions of n-3 PUFAs on endothelial function may counteract the endothelial toxicity of substances such as Hcy, but only few and short-term studies have been published on the effects of n-3 PUFAs on Hcy [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Reduction in Homocysteine by n–3 Polyunsaturated Fatty Acids after 1 Year in a Randomised Double-Blind Study following an Acute Myocardial Infarction: No Effect on Endothelial Adhesion Properties

Grundt

Nilsen

Mansoor³

et al. 2003

Pathophysiol Haemos Thromb

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We hypothesized that n–3 polyunsaturated fatty acids (n–3 PUFAs) as compared to corn oil administered for 1 year following an acute myocardial infarction (MI) may reduce plasma total homocysteine (p-tHcy), ultrasensitive C-reactive protein (µCRP), and the adhesive properties of the endothelium, expressed as soluble E-selectin (sE-selectin) and soluble intercellular adhesion molecule-1 (sICAM-1). In a prospective, randomised, double-blind study, 300 acute MI patients were allocated to highly concentrated n–3 PUFAs (n = 150) or corn oil (n = 150). After 1 year on treatment there was an intergroup difference in p-tHcy in favour of the n–3 group (n = 118), p = 0.022. However, sE-selectin, sICAM-1 and µCRP were unaffected by the treatment. In conclusion, reduction of p-tHcy by long-term n–3 PUFAs treatment was not associated with demonstrable effects on markers of endothelial adhesion properties.

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“…22 A negative correlation between high Hcy levels and PPAR expression has been suggested in humans. 23 In a murine model of HHcy, PPAR␣ was shown to ameliorate endothelial dysfunction. 24 In this study, we used our Mthfr-deficient mouse model to study the potential interaction between homocysteine and lipid metabolism.…”

mentioning

confidence: 99%

Elevated Homocysteine Reduces Apolipoprotein A-I Expression in Hyperhomocysteinemic Mice and in Males With Coronary Artery Disease

Mikael

Genest

Rozen

2006

Circulation Research

152

136

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Abstract-Hyperhomocysteinemia, a risk factor for cardiovascular disease, is caused by nutritional or genetic disturbances in homocysteine metabolism. A polymorphism in methylenetetrahydrofolate reductase (MTHFR) is the most common genetic cause of mild hyperhomocysteinemia. To examine mechanisms by which an elevation in plasma homocysteine leads to vascular disease, we first performed microarray analyses in livers of Mthfr-deficient mice and identified differentially expressed genes that are involved in lipid and cholesterol metabolism. Microarrays and RT-PCR showed decreased mRNA for apolipoprotein A (ApoA)-IV and for ApoA-I and increased mRNA for cholesterol 7␣ hydroxylase (Cyp7A1) in Mthfr ϩ/Ϫ mice compared with Mthfr ϩ/ϩ mice. Western blotting revealed that ApoA-I protein levels in liver and plasma of Mthfr ϩ/Ϫ mice were 52% and 62% of levels in the respective tissues of Mthfr ϩ/ϩ mice. We also performed Western analysis for plasma ApoA-I protein levels in 60 males with coronary artery disease and identified a significant (PϽ0.01) negative correlation (Ϫ0.33) between ApoA-I and plasma homocysteine levels. This cohort also displayed a negative correlation (Ϫ0.24, Pϭ0.06) between high-density lipoprotein cholesterol and plasma homocysteine. Key Words: homocysteine Ⅲ methylenetetrahydrofolate reductase Ⅲ apolipoprotein A-I Ⅲ high-density lipoprotein Ⅲ peroxisome proliferator-activated receptor ␣ C onventional risk factors for cardiovascular disease including hypercholesterolemia, hypertension, smoking, and diabetes account for approximately 50% of all cases. 1 Evidence now indicates that hyperhomocysteinemia (HHcy), which occurs in Ϸ5% to 7% of the general population, is an important risk factor for atherosclerotic and thrombotic disease. 2 The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) plays a critical role in regulating total homocysteine (tHcy) levels by synthesizing 5-methyltetrahydrofolate, which provides the methyl group for homocysteine remethylation to methionine. Mild deficiency of MTHFR, the most common genetic cause of mild HHcy, occurs frequently in many populations (10% to 15% of individuals) and is attributable to homozygosity for a polymorphism (677C3 T) that reduces enzyme activity. 3 To generate an animal model for HHcy, we had created mice with a heterozygous (ϩ/Ϫ) disruption of the Mthfr gene. 4 With Ϸ50% residual activity and Ϸ1.7-fold greater levels of plasma tHcy compared with their wild-type (ϩ/ϩ) littermates (5.4Ϯ1.0 versus 3.2Ϯ1.2, meanϮSD), 4 the Mthfr

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Plasma homocysteine concentration related to diet, endothelial function and mononuclear cell gene expression among male hyperlipidaemic smokers

Cited by 53 publications

References 61 publications

Serum homocysteine is weakly associated with von Willebrand factor and soluble vascular cell adhesion molecule 1, but not with C‐reactive protein in type 2 diabetic and non‐diabetic subjects — The Hoorn Study

Serum homocysteine is weakly associated with von Willebrand factor and soluble vascular cell adhesion molecule 1, but not with C‐reactive protein in type 2 diabetic and non‐diabetic subjects — The Hoorn Study

Reduction in Homocysteine by n–3 Polyunsaturated Fatty Acids after 1 Year in a Randomised Double-Blind Study following an Acute Myocardial Infarction: No Effect on Endothelial Adhesion Properties

Elevated Homocysteine Reduces Apolipoprotein A-I Expression in Hyperhomocysteinemic Mice and in Males With Coronary Artery Disease

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