Abstract
The generation by genetic engineering of two murine models to investigate atherosclerosis, such as the apoE- and LDLr- deficient mice, is providing an extraordinaire knowledge of the effect of different nutrients on this complex disease. The present revision provides a comprehensive overview of the advances in this field that point to a remarkable complexity. While some controversies over puzzling results could be explained invoking potential nutrient interactions or different food sources of nutrients, it also appears that other factors such as sex, genetic background or immunological status are emerging as generators of differential responses to nutrients during the atherosclerotic process.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alcohol Drinking
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Allergy and Immunology
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Animals
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Antioxidants / chemistry
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Apolipoproteins E / genetics
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Arginine / chemistry
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Arteriosclerosis
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Ascorbic Acid / chemistry
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Atherosclerosis / genetics*
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Atherosclerosis / pathology*
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Cell Proliferation
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Dietary Fats
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Disease Models, Animal*
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Energy Metabolism
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Fatty Acids, Monounsaturated / metabolism
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Fatty Acids, Unsaturated / metabolism
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Genetic Engineering*
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Genetic Variation
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Genomics
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Homocysteine / chemistry
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Insulin Resistance
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Iron / metabolism
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Magnesium / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Models, Biological
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Models, Genetic
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Phytosterols / chemistry
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Phytosterols / metabolism
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Receptors, LDL / metabolism
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Sex Factors
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Sodium / metabolism
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Taurine / chemistry
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Vitamin E / chemistry
Substances
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Antioxidants
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Apolipoproteins E
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Dietary Fats
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Fatty Acids, Monounsaturated
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Fatty Acids, Unsaturated
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Phytosterols
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Receptors, LDL
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Homocysteine
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Vitamin E
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Taurine
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Arginine
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Sodium
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Iron
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Magnesium
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Ascorbic Acid