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Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)

Background: Dietary silicon has been positively linked with vascular health and protection against atherosclerotic plaque formation, but the mechanism of action is unclear. Objectives: We investigated the effect of dietary silicon on 1) serum and aorta silicon concentrations, 2) the development of a...

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Autores principales: Jugdaohsingh, Ravin, Kessler, Katharina, Messner, Barbara, Stoiber, Martin, Pedro, Liliana D, Schima, Heinrich, Laufer, Günther, Powell, Jonathan J, Bernhard, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Nutrition 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478943/
https://www.ncbi.nlm.nih.gov/pubmed/25972522
http://dx.doi.org/10.3945/jn.114.206193
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author Jugdaohsingh, Ravin
Kessler, Katharina
Messner, Barbara
Stoiber, Martin
Pedro, Liliana D
Schima, Heinrich
Laufer, Günther
Powell, Jonathan J
Bernhard, David
author_facet Jugdaohsingh, Ravin
Kessler, Katharina
Messner, Barbara
Stoiber, Martin
Pedro, Liliana D
Schima, Heinrich
Laufer, Günther
Powell, Jonathan J
Bernhard, David
author_sort Jugdaohsingh, Ravin
collection PubMed
description Background: Dietary silicon has been positively linked with vascular health and protection against atherosclerotic plaque formation, but the mechanism of action is unclear. Objectives: We investigated the effect of dietary silicon on 1) serum and aorta silicon concentrations, 2) the development of aortic lesions and serum lipid concentrations, and 3) the structural and biomechanic properties of the aorta. Methods: Two studies, of the same design, were conducted to address the above objectives. Female mice, lacking the apolipoprotein E (apoE) gene, and therefore susceptible to atherosclerosis, were separated into 3 groups of 10–15 mice, each exposed to a high-fat diet (21% wt milk fat and 1.5% wt cholesterol) but with differing concentrations of dietary silicon, namely: silicon-deprived (−Si; <3-μg silicon/g feed), silicon-replete in feed (+Si-feed; 100-μg silicon/g feed), and silicon-replete in drinking water (+Si-water; 115-μg silicon/mL) for 15–19 wk. Silicon supplementation was in the form of sodium metasilicate (feed) or monomethylsilanetriol (drinking water). Results: The serum silicon concentration in the −Si group was significantly lower than in the +Si-feed (by up to 78%; P < 0.003) and the +Si-water (by up to 84%; P < 0.006) groups. The aorta silicon concentration was also lower in the −Si group than in the +Si-feed group (by 65%; P = 0.025), but not compared with the +Si-water group. There were no differences in serum and aorta silicon concentrations between the silicon-replete groups. Body weights, tissue wet weights at necropsy, and structural, biomechanic, and morphologic properties of the aorta were not affected by dietary silicon; nor were the development of fatty lesions and serum lipid concentrations. Conclusions: These findings suggest that dietary silicon has no effect on atherosclerosis development and vascular health in the apoE mouse model of diet-induced atherosclerosis, contrary to the reported findings in the cholesterol-fed rabbit model.
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spelling pubmed-44789432015-07-09 Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3) Jugdaohsingh, Ravin Kessler, Katharina Messner, Barbara Stoiber, Martin Pedro, Liliana D Schima, Heinrich Laufer, Günther Powell, Jonathan J Bernhard, David J Nutr Nutrient Requirements and Optimal Nutrition Background: Dietary silicon has been positively linked with vascular health and protection against atherosclerotic plaque formation, but the mechanism of action is unclear. Objectives: We investigated the effect of dietary silicon on 1) serum and aorta silicon concentrations, 2) the development of aortic lesions and serum lipid concentrations, and 3) the structural and biomechanic properties of the aorta. Methods: Two studies, of the same design, were conducted to address the above objectives. Female mice, lacking the apolipoprotein E (apoE) gene, and therefore susceptible to atherosclerosis, were separated into 3 groups of 10–15 mice, each exposed to a high-fat diet (21% wt milk fat and 1.5% wt cholesterol) but with differing concentrations of dietary silicon, namely: silicon-deprived (−Si; <3-μg silicon/g feed), silicon-replete in feed (+Si-feed; 100-μg silicon/g feed), and silicon-replete in drinking water (+Si-water; 115-μg silicon/mL) for 15–19 wk. Silicon supplementation was in the form of sodium metasilicate (feed) or monomethylsilanetriol (drinking water). Results: The serum silicon concentration in the −Si group was significantly lower than in the +Si-feed (by up to 78%; P < 0.003) and the +Si-water (by up to 84%; P < 0.006) groups. The aorta silicon concentration was also lower in the −Si group than in the +Si-feed group (by 65%; P = 0.025), but not compared with the +Si-water group. There were no differences in serum and aorta silicon concentrations between the silicon-replete groups. Body weights, tissue wet weights at necropsy, and structural, biomechanic, and morphologic properties of the aorta were not affected by dietary silicon; nor were the development of fatty lesions and serum lipid concentrations. Conclusions: These findings suggest that dietary silicon has no effect on atherosclerosis development and vascular health in the apoE mouse model of diet-induced atherosclerosis, contrary to the reported findings in the cholesterol-fed rabbit model. American Society for Nutrition 2015-07 2015-05-13 /pmc/articles/PMC4478943/ /pubmed/25972522 http://dx.doi.org/10.3945/jn.114.206193 Text en http://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the CC-BY license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Nutrient Requirements and Optimal Nutrition
Jugdaohsingh, Ravin
Kessler, Katharina
Messner, Barbara
Stoiber, Martin
Pedro, Liliana D
Schima, Heinrich
Laufer, Günther
Powell, Jonathan J
Bernhard, David
Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title_full Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title_fullStr Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title_full_unstemmed Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title_short Dietary Silicon Deficiency Does Not Exacerbate Diet-Induced Fatty Lesions in Female ApoE Knockout Mice(1)(2)(3)
title_sort dietary silicon deficiency does not exacerbate diet-induced fatty lesions in female apoe knockout mice(1)(2)(3)
topic Nutrient Requirements and Optimal Nutrition
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478943/
https://www.ncbi.nlm.nih.gov/pubmed/25972522
http://dx.doi.org/10.3945/jn.114.206193
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