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

Relevy NZ, Harats D, Harari A, Ben-Amotz A, Bitzur R, Rühl R, Shaish A - Biomed Res Int (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

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

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.

No MeSH data available.


Related in: MedlinePlus

Mouse body weight throughout the study. Mice were weighed every week (Exp. 1). A trend towards lower body weight was noted in the VAD group (P = 0.072). Values are means ± SE, n = 15-16. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).
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fig1: Mouse body weight throughout the study. Mice were weighed every week (Exp. 1). A trend towards lower body weight was noted in the VAD group (P = 0.072). Values are means ± SE, n = 15-16. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).

Mentions: The aim of the study was to investigate whether a vitamin A-deficient diet accelerates atherogenesis in apoE−/− mice and to examine whether fortification of this diet with a Dunaliella powder rich in β-carotene isomers, as a sole source of dietary provitamin A, would compensate for dietary vitamin A deficiency. We placed 68 apoE−/− male mice (Exp. 1) for 15 weeks on the following diet regimes: chow diet (control); Dunaliella powder-fortified diet, as a natural source for β-carotene isomers (BC), vitamin A-deficient diet (VAD), and vitamin A-deficient diet fortified with Dunaliella powder (VAD-BC). Vitamin A deficiency did not significantly affect weight gain, although a trend towards lower weight was noted in the VAD group (P = 0.072), while weight gain in the BC-fortified groups was similar to the control group (Figure 1).


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

Relevy NZ, Harats D, Harari A, Ben-Amotz A, Bitzur R, Rühl R, Shaish A - Biomed Res Int (2015)

Mouse body weight throughout the study. Mice were weighed every week (Exp. 1). A trend towards lower body weight was noted in the VAD group (P = 0.072). Values are means ± SE, n = 15-16. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4352738&req=5

fig1: Mouse body weight throughout the study. Mice were weighed every week (Exp. 1). A trend towards lower body weight was noted in the VAD group (P = 0.072). Values are means ± SE, n = 15-16. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).
Mentions: The aim of the study was to investigate whether a vitamin A-deficient diet accelerates atherogenesis in apoE−/− mice and to examine whether fortification of this diet with a Dunaliella powder rich in β-carotene isomers, as a sole source of dietary provitamin A, would compensate for dietary vitamin A deficiency. We placed 68 apoE−/− male mice (Exp. 1) for 15 weeks on the following diet regimes: chow diet (control); Dunaliella powder-fortified diet, as a natural source for β-carotene isomers (BC), vitamin A-deficient diet (VAD), and vitamin A-deficient diet fortified with Dunaliella powder (VAD-BC). Vitamin A deficiency did not significantly affect weight gain, although a trend towards lower weight was noted in the VAD group (P = 0.072), while weight gain in the BC-fortified groups was similar to the control group (Figure 1).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

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

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.

No MeSH data available.


Related in: MedlinePlus