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维生素A缺乏饮食加速了载脂蛋白E基因敲除小鼠的动脉粥样硬化形成,而饮食中的β-胡萝卜素可预防这种后果。

Vitamin A-deficient diet accelerated atherogenesis in apolipoprotein E(-/-) mice and dietary β-carotene prevents this consequence.

作者信息

Relevy Noa Zolberg, Harats Dror, Harari Ayelet, Ben-Amotz Ami, Bitzur Rafael, Rühl Ralph, Shaish Aviv

机构信息

The Bert W. Strassburger Lipid Center, Sheba Medical Center, 5265601 Tel-Hashomer, Israel ; Sackler Faculty of Medicine, Tel-Aviv University, Israel.

The Bert W. Strassburger Lipid Center, Sheba Medical Center, 5265601 Tel-Hashomer, Israel.

出版信息

Biomed Res Int. 2015;2015:758723. doi: 10.1155/2015/758723. Epub 2015 Feb 23.

DOI:10.1155/2015/758723
PMID:25802864
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4352738/
Abstract

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.

摘要

维生素A参与葡萄糖浓度调节、脂质代谢和炎症反应,而这些都是动脉粥样硬化形成的主要危险因素。然而,维生素A缺乏对动脉粥样硬化形成的影响尚未得到研究。因此,本研究的目的是检验维生素A缺乏是否会加速载脂蛋白E缺陷小鼠(apoE(-/-))的动脉粥样硬化进程。将apoE(-/-)小鼠分为以下几组:对照组,喂食含维生素A的普通饲料;BC组,喂食添加含βc异构体的杜氏藻粉的普通饲料;VAD组,喂食维生素A缺乏饲料;VAD-BC组,喂食添加杜氏藻粉的维生素A缺乏饲料。经过15周的治疗后,VAD组肝脏视黄醇浓度显著下降,降至对照组的约30%。与对照组相比,维生素A缺乏饲料显著增加了血浆胆固醇浓度以及主动脉窦处的动脉粥样硬化病变面积(增加61%)。饲料中添加βc可抑制喂食维生素A缺乏饲料小鼠的血浆胆固醇升高,并延缓动脉粥样硬化进程。结果表明,应将膳食维生素A缺乏作为动脉粥样硬化的一个危险因素进行研究,并且膳食βc作为类视黄醇的唯一来源,可以弥补维生素A缺乏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/598efa7911bc/BMRI2015-758723.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/004d9494cfbd/BMRI2015-758723.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/32defe0cb8bc/BMRI2015-758723.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/07e6111f8612/BMRI2015-758723.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/833fa733c403/BMRI2015-758723.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/598efa7911bc/BMRI2015-758723.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/004d9494cfbd/BMRI2015-758723.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/32defe0cb8bc/BMRI2015-758723.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/07e6111f8612/BMRI2015-758723.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/833fa733c403/BMRI2015-758723.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ab6/4352738/598efa7911bc/BMRI2015-758723.005.jpg

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