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Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence
Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whet...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352738/ https://www.ncbi.nlm.nih.gov/pubmed/25802864 http://dx.doi.org/10.1155/2015/758723 |
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author | Relevy, Noa Zolberg Harats, Dror Harari, Ayelet Ben-Amotz, Ami Bitzur, Rafael Rühl, Ralph Shaish, Aviv |
author_facet | Relevy, Noa Zolberg Harats, Dror Harari, Ayelet Ben-Amotz, Ami Bitzur, Rafael Rühl, Ralph Shaish, Aviv |
author_sort | Relevy, Noa Zolberg |
collection | PubMed |
description | Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE(−/−)). ApoE(−/−) mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified with Dunaliella powder containing βc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with a Dunaliella powder. Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietary βc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet. The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietary βc, as a sole source of retinoids, can compensate for vitamin A deficiency. |
format | Online Article Text |
id | pubmed-4352738 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-43527382015-03-23 Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence Relevy, Noa Zolberg Harats, Dror Harari, Ayelet Ben-Amotz, Ami Bitzur, Rafael Rühl, Ralph Shaish, Aviv Biomed Res Int Research Article Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE(−/−)). ApoE(−/−) mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified with Dunaliella powder containing βc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with a Dunaliella powder. Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietary βc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet. The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietary βc, as a sole source of retinoids, can compensate for vitamin A deficiency. Hindawi Publishing Corporation 2015 2015-02-23 /pmc/articles/PMC4352738/ /pubmed/25802864 http://dx.doi.org/10.1155/2015/758723 Text en Copyright © 2015 Noa Zolberg Relevy et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Relevy, Noa Zolberg Harats, Dror Harari, Ayelet Ben-Amotz, Ami Bitzur, Rafael Rühl, Ralph Shaish, Aviv Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title | Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title_full | Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title_fullStr | Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title_full_unstemmed | Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title_short | Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E(−/−) Mice and Dietary β-Carotene Prevents This Consequence |
title_sort | vitamin a-deficient diet accelerated atherogenesis in apolipoprotein e(−/−) mice and dietary β-carotene prevents this consequence |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352738/ https://www.ncbi.nlm.nih.gov/pubmed/25802864 http://dx.doi.org/10.1155/2015/758723 |
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