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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

Plasma cholesterol concentrations. Plasma cholesterol concentrations (a) and lipoprotein cholesterol content (b). Mice fed chow or vitamin A-deficient diet with or without βC after 15 weeks of treatment. VAD significantly increased plasma cholesterol concentrations due to increased levels of non-HDL cholesterol. Values are means ± SE, n = 15-16. a, bWithin the graph, means without a common letter differ, P < 0.05. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).
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fig3: Plasma cholesterol concentrations. Plasma cholesterol concentrations (a) and lipoprotein cholesterol content (b). Mice fed chow or vitamin A-deficient diet with or without βC after 15 weeks of treatment. VAD significantly increased plasma cholesterol concentrations due to increased levels of non-HDL cholesterol. Values are means ± SE, n = 15-16. a, bWithin the graph, means without a common letter differ, P < 0.05. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).

Mentions: Vitamin A-deficient diet significantly increased plasma cholesterol concentrations and FPLC analysis showed that this increase is due to higher concentrations of the atherogenic, non-HDL cholesterol. Dietary β-carotene fortification suppressed this elevation, and plasma cholesterol concentrations in the BC and VAD-BC groups were lower throughout the experiments compared to the control or the VAD group, respectively (Figure 3). The atherosclerotic lesion area was quantified at the aortic sinus by oil-red O staining of the lipids. The red color indicates the presence of atherosclerotic lesions (Figure 5(b)). The vitamin A-deficient diet significantly increased (61%) the atherosclerotic lesion area at the aortic sinus compared to the control group (Figure 4). Remarkably, although β-carotene did not restore the liver retinol pool, it significantly inhibited atherogenesis in mice fed a vitamin A-deficient diet, and the lesion area was similar to the control group fed the vitamin A-containing diet.


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)

Plasma cholesterol concentrations. Plasma cholesterol concentrations (a) and lipoprotein cholesterol content (b). Mice fed chow or vitamin A-deficient diet with or without βC after 15 weeks of treatment. VAD significantly increased plasma cholesterol concentrations due to increased levels of non-HDL cholesterol. Values are means ± SE, n = 15-16. a, bWithin the graph, means without a common letter differ, P < 0.05. 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

fig3: Plasma cholesterol concentrations. Plasma cholesterol concentrations (a) and lipoprotein cholesterol content (b). Mice fed chow or vitamin A-deficient diet with or without βC after 15 weeks of treatment. VAD significantly increased plasma cholesterol concentrations due to increased levels of non-HDL cholesterol. Values are means ± SE, n = 15-16. a, bWithin the graph, means without a common letter differ, P < 0.05. Dunaliella treated group (BC); vitamin A-deficient diet group (VAD); vitamin A-deficient diet fortified with Dunaliella group (VAD-BC).
Mentions: Vitamin A-deficient diet significantly increased plasma cholesterol concentrations and FPLC analysis showed that this increase is due to higher concentrations of the atherogenic, non-HDL cholesterol. Dietary β-carotene fortification suppressed this elevation, and plasma cholesterol concentrations in the BC and VAD-BC groups were lower throughout the experiments compared to the control or the VAD group, respectively (Figure 3). The atherosclerotic lesion area was quantified at the aortic sinus by oil-red O staining of the lipids. The red color indicates the presence of atherosclerotic lesions (Figure 5(b)). The vitamin A-deficient diet significantly increased (61%) the atherosclerotic lesion area at the aortic sinus compared to the control group (Figure 4). Remarkably, although β-carotene did not restore the liver retinol pool, it significantly inhibited atherogenesis in mice fed a vitamin A-deficient diet, and the lesion area was similar to the control group fed the vitamin A-containing diet.

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