Attenuation of atherogenic apo B-48-dependent hyperlipidemia and high density lipoprotein remodeling induced by vitamin C and E combination and their beneficial effect on lethal ischemic heart disease in mice

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Background and aims

Atherosclerotic cardiovascular disease is highly prevalent and its underlying pathogenesis involves dyslipidemia including pro-atherogenic high density lipoprotein (HDL) remodeling. Vitamins C and E have been proposed as atheroprotective agents for cardiovascular disease management. However, their effects and benefits on high density lipoprotein function and remodeling are unknown. In this study, we evaluated the role of vitamin C and E on non HDL lipoproteins as well as HDL function and remodeling, along with their effects on inflammation/oxidation biomarkers and atherosclerosis in atherogenic diet-fed SR-B1 KO/ApoER61 ^h/h mice.

Methods and results

Mice were pre-treated for 5 weeks before and during atherogenic diet feeding with vitamin C and E added to water and diet, respectively. Compared to a control group, combined vitamin C and E administration reduced serum total cholesterol and triglyceride levels by decreasing apo B-48-containing lipoproteins, remodeled HDL particles by reducing phospholipid as well as increasing PON1 and apo D content, and diminished PLTP activity and levels. Vitamin supplementation improved HDL antioxidant function and lowered serum TNF-α levels. Vitamin C and E combination attenuated atherogenesis and increased lifespan in atherogenic diet-fed SR-B1 KO/ApoER61 ^h/h mice.

Conclusions

Vitamin C and E administration showed significant lipid metabolism regulating effects, including HDL remodeling and decreased levels of apoB-containing lipoproteins, in mice. In addition, this vitamin supplementation generated a cardioprotective effect in a murine model of severe and lethal atherosclerotic ischemic heart disease.

Related collections

Most cited references 35

Record: found
Abstract: found
Article: not found

Vitamin E consumption and the risk of coronary heart disease in men.

E B Rimm, M Stampfer, A Ascherio … (1993)

The oxidative modification of low-density lipoproteins increases their incorporation into the arterial intima, an essential step in atherogenesis. Although dietary antioxidants, such as vitamin C, carotene, and vitamin E, have been hypothesized to prevent coronary heart disease, prospective epidemiologic data are sparse. In 1986, 39,910 U.S. male health professionals 40 to 75 years of age who were free of diagnosed coronary heart disease, diabetes, and hypercholesterolemia completed detailed dietary questionnaires that assessed their usual intake of vitamin C, carotene, and vitamin E in addition to other nutrients. During four years of follow-up, we documented 667 cases of coronary disease. After controlling for age and several coronary risk factors, we observed a lower risk of coronary disease among men with higher intakes of vitamin E (P for trend = 0.003). For men consuming more than 60 IU per day of vitamin E, the multivariate relative risk was 0.64 (95 percent confidence interval, 0.49 to 0.83) as compared with those consuming less than 7.5 IU per day. As compared with men who did not take vitamin E supplements, men who took at least 100 IU per day for at least two years had a multivariate relative risk of coronary disease of 0.63 (95 percent confidence interval, 0.47 to 0.84). Carotene intake was not associated with a lower risk of coronary disease among those who had never smoked, but it was inversely associated with the risk among current smokers (relative risk, 0.30; 95 percent confidence interval, 0.11 to 0.82) and former smokers (relative risk, 0.60; 95 percent confidence interval, 0.38 to 0.94). In contrast, a high intake of vitamin C was not associated with a lower risk of coronary disease. These data do not prove a causal relation, but they provide evidence of an association between a high intake of vitamin E and a lower risk of coronary heart disease in men. Public policy recommendations with regard to the use of vitamin E supplements should await the results of additional studies.

0 comments Cited 266 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Inflammatory remodeling of the HDL proteome impairs cholesterol efflux capacity.

Tomas Vaisar, Chongren Tang, Ilona Babenko … (2015)

Recent studies demonstrate that HDL's ability to promote cholesterol efflux from macrophages associates strongly with cardioprotection in humans independently of HDL-cholesterol (HDL-C) and apoA-I, HDL's major protein. However, the mechanisms that impair cholesterol efflux capacity during vascular disease are unclear. Inflammation, a well-established risk factor for cardiovascular disease, has been shown to impair HDL's cholesterol efflux capacity. We therefore tested the hypothesis that HDL's impaired efflux capacity is mediated by specific changes of its protein cargo. Humans with acute inflammation induced by low-level endotoxin had unchanged HDL-C levels, but their HDL-C efflux capacity was significantly impaired. Proteomic analyses demonstrated that HDL's cholesterol efflux capacity correlated inversely with HDL content of serum amyloid A (SAA)1 and SAA2. In mice, acute inflammation caused a marked impairment of HDL-C efflux capacity that correlated with a large increase in HDL SAA. In striking contrast, the efflux capacity of mouse inflammatory HDL was preserved with genetic ablation of SAA1 and SAA2. Our observations indicate that the inflammatory impairment of HDL-C efflux capacity is due in part to SAA-mediated remodeling of HDL's protein cargo.

0 comments Cited 76 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Vitamin E suppresses isoprostane generation in vivo and reduces atherosclerosis in ApoE-deficient mice.

Stephen Rader, J Rokach, Erich Fitzgerald … (1998)

Oxidative modification of low density lipoprotein (LDL) has been implicated in atherogenesis. Evidence consistent with this hypothesis includes the presence of oxidized lipids in atherosclerotic lesions, the newly discovered biological properties conferred on LDL by oxidation and the acceleration of atherogenesis by in vivo delivery of the gene for 15-lipoxygenase, an oxidizing enzyme present in atherosclerotic lesions. However, it is still unknown whether oxidative stress actually coincides with the evolution of the disease or whether it is of functional relevance to atherogenesis in vivo. Isoprostanes are products of arachidonic acid catalyzed by free radicals, which reflect oxidative stress and lipid peroxidation in vivo. Elevation of tissue and urinary isoprostanes is characteristic of human atherosclerosis. Here, deficiency in apolipoprotein E in the mouse (apoE-/-) resulted in atherogenesis and an increase in iPF2alpha-VI, an F2-isoprostane, in urine, plasma and vascular tissue. Supplementation with vitamin E significantly reduced isoprostane generation, but had no effect on plasma cholesterol levels in apoE-/- mice. Aortic lesion areas and iPF2alpha-VI levels in the arterial wall were also reduced significantly by vitamin E. Our results indicate that oxidative stress is increased in the apoE-/- mouse, is of functional importance in the evolution of atherosclerosis and can be suppressed by oral administration of vitamin E.

0 comments Cited 50 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

S. Contreras-Duarte: secontre@uc.cl

P. Chen: pxchen@uc.cl

M. Andía: mandia@med.puc.cl

S. Uribe: suribe@med.puc.cl

P. Irarrázaval: pim@ing.puc.cl

S. Kopp: susanne.kopp@medunigraz.at

S. Kern: sabine.kern@medunigraz.at

G. Marsche: gunther.marsche@medunigraz.at

D. Busso: dbusso@med.puc.cl

C. Wadsack: christian.wadsack@medunigraz.at

A. Rigotti: +56 2 2354 3836 , arigotti@med.puc.cl

Journal

Journal ID (nlm-ta): Biol Res

Journal ID (iso-abbrev): Biol. Res

Title: Biological Research

Publisher: BioMed Central (London )

ISSN (Print): 0716-9760

ISSN (Electronic): 0717-6287

Publication date (Electronic): 15 September 2018

Publication date PMC-release: 15 September 2018

Publication date Collection: 2018

Volume: 51

Electronic Location Identifier: 34

Affiliations

[1 ]ISNI 0000 0001 2157 0406, GRID grid.7870.8, Department of Nutrition, Diabetes and Metabolism, School of Medicine, , Pontificia Universidad Católica de Chile, ; Diagonal Paraguay #362 - 4º, Piso, 8330024 Santiago, Chile

[2 ]ISNI 0000 0001 2157 0406, GRID grid.7870.8, Department of Radiology, School of Medicine, , Pontificia Universidad Católica de Chile, ; Santiago, Chile

[3 ]ISNI 0000 0001 2157 0406, GRID grid.7870.8, Center of Molecular Nutrition and Chronic Diseases, School of Medicine, , Pontificia Universidad Católica de Chile, ; Santiago, Chile

[4 ]ISNI 0000 0001 2157 0406, GRID grid.7870.8, Biomedical Imaging Center, School of Engineering, , Pontificia Universidad Católica de Chile, ; Santiago, Chile

[5 ]ISNI 0000 0001 2157 0406, GRID grid.7870.8, Department of Electrical Engineering, School of Engineering, , Pontificia Universidad Católica de Chile, ; Santiago, Chile

[6 ]ISNI 0000 0000 8988 2476, GRID grid.11598.34, Department of Obstetrics and Gynecology, , Medical University of Graz, ; Graz, Austria

[7 ]ISNI 0000 0000 8988 2476, GRID grid.11598.34, Institute of Experimental and Clinical Pharmacology, , Medical University of Graz, ; Graz, Austria

Article

Publisher ID: 183

DOI: 10.1186/s40659-018-0183-6

PMC ID: 6138920

PubMed ID: 30219096

SO-VID: a0918744-d49c-43f9-9cae-08c3d6a3e70a

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 20 May 2018

Date accepted : 6 September 2018

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100002850, Fondo Nacional de Desarrollo Científico y Tecnológico;

Award ID: 1110712-1150399

Award ID: 21120282

Award ID: 1141236

Award ID: ACT1416

Award Recipient : S. Contreras-Duarte P. Irarrázaval D. Busso A. Rigotti

Funded by: FundRef http://dx.doi.org/10.13039/501100004955, Österreichische Forschungsförderungsgesellschaft;

Award ID: 4354192

Award Recipient : C. Wadsack

Custom metadata

Keywords: hdl,vitamin c and e,serum lipids,atherosclerosis

Data availability:

Keywords: hdl, vitamin c and e, serum lipids, atherosclerosis

Comments

Comment on this article

scite_

Cited by 11

See all cited by

Most referenced authors 1,111

See all reference authors

Attenuation of atherogenic apo B-48-dependent hyperlipidemia and high density lipoprotein remodeling induced by vitamin C and E combination and their beneficial effect on lethal ischemic heart disease in mice

Read this article at

Abstract

Background and aims

Methods and results

Conclusions

Related collections

SciELO Chile

Most cited references 35

Vitamin E consumption and the risk of coronary heart disease in men.

Inflammatory remodeling of the HDL proteome impairs cholesterol efflux capacity.

Vitamin E suppresses isoprostane generation in vivo and reduces atherosclerosis in ApoE-deficient mice.

Author and article information

Contributors

Journal

Affiliations

Article

History

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 287

Cited by 11

Most referenced authors 1,111