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Published in: BMC Cardiovascular Disorders 1/2016

Open Access 01-12-2016 | Research article

Hyperhomocysteinemia is associated with decreased apolipoprotein AI levels in normal healthy people

Authors: Ying Wang, Jia Liu, Yuliang Jiang, Heng Zhang, Song Leng, Guang Wang

Published in: BMC Cardiovascular Disorders | Issue 1/2016

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Abstract

Background

Hyperhomocysteinemia (HHcy) is an independent risk factor for various cardiovascular diseases. Animal studies have shown that homocysteine (Hcy) inhibits hepatic expression of apolipoprotein AI (apoAI). Our recent clinical study showed that increased plasma Hcy levels were associated with decreased apoAI levels in patients with impaired glucose tolerance. In this study, we assessed a potential association between Hcy and apoAI levels in normal healthy people.

Methods

A total of 1768 normal healthy individuals were divided into two groups: the control group (subjects without HHcy) and the HHcy group (subjects with HHcy).

Results

HHcy subjects exhibited significantly lower high-density lipoprotein cholesterol (HDL-C) and apoAI levels than the control group (HDL-C: 1.18 ± 0.25 vs. 1.29 ± 0.32 mmol/L; apoAI: 1.38 ± 0.19 vs. 1.47 ± 0.25 g/L; all P < 0.01). Plasma Hcy levels were negatively associated with HDL-C and apoAI levels after adjustments for age, BMI and TG (HDL-C: r = –0.10; apoAI: r = –0.11; all P < 0.05). Multivariate regression analysis showed that the plasma Hcy levels were an independent influencing factor for apoAI (β = –0.065, P < 0.05).

Conclusions

Increased plasma Hcy levels were associated with decreased apoAI levels in normal healthy people, and the inhibition of apoAI synthesis might be a mechanism through which Hcy is linked with the development of atherosclerosis in HHcy subjects.
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Metadata
Title
Hyperhomocysteinemia is associated with decreased apolipoprotein AI levels in normal healthy people
Authors
Ying Wang
Jia Liu
Yuliang Jiang
Heng Zhang
Song Leng
Guang Wang
Publication date
01-12-2016
Publisher
BioMed Central
Published in
BMC Cardiovascular Disorders / Issue 1/2016
Electronic ISSN: 1471-2261
DOI
https://doi.org/10.1186/s12872-016-0186-6

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