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Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.

Near-isocaloric diets with qualitative and quantitative differences in fat content have a profound influence on the manifestation and progression of the autoimmune syndrome that occurs in female MRL/lpr mice. In these animals, a high (9%) lipid intake resulted in a significantly higher mortality rat...

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Autors principals: Morrow, W J, Homsy, J, Swanson, C A, Ohashi, Y, Estes, J, Levy, J A
Format: Article
Idioma:English
Publicat: 1986
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Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC1453202/
https://ncbi.nlm.nih.gov/pubmed/3491785
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spelling pubmed-14532022007-02-06 Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice. Morrow, W J Homsy, J Swanson, C A Ohashi, Y Estes, J Levy, J A Immunology Research Article Near-isocaloric diets with qualitative and quantitative differences in fat content have a profound influence on the manifestation and progression of the autoimmune syndrome that occurs in female MRL/lpr mice. In these animals, a high (9%) lipid intake resulted in a significantly higher mortality rate: 60% (saturated fat) and 75% (unsaturated fat) compared to 35% at 1 year for a group fed a diet low in fat. Furthermore, beginning at 7 months of age mice from both of the high fat diet groups exhibited a significantly higher incidence of proteinuria than mice in the low fat group. Immunologically, the group fed the high unsaturated fat diet had the highest incidence of anti-dsDNA autoantibodies, and the high saturated fat group had the poorest macrophage phagocytic function. The low fat diet preserved near 'normal' immune function in general, particularly IL-2 production. No significant differences were noted in either the production of rheumatoid factor or natural killer cell activity, irrespective of age or diet. 1986-11 /pmc/articles/PMC1453202/ /pubmed/3491785 Text en
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Research Article
spellingShingle Research Article
Morrow, W J
Homsy, J
Swanson, C A
Ohashi, Y
Estes, J
Levy, J A
Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
description Near-isocaloric diets with qualitative and quantitative differences in fat content have a profound influence on the manifestation and progression of the autoimmune syndrome that occurs in female MRL/lpr mice. In these animals, a high (9%) lipid intake resulted in a significantly higher mortality rate: 60% (saturated fat) and 75% (unsaturated fat) compared to 35% at 1 year for a group fed a diet low in fat. Furthermore, beginning at 7 months of age mice from both of the high fat diet groups exhibited a significantly higher incidence of proteinuria than mice in the low fat group. Immunologically, the group fed the high unsaturated fat diet had the highest incidence of anti-dsDNA autoantibodies, and the high saturated fat group had the poorest macrophage phagocytic function. The low fat diet preserved near 'normal' immune function in general, particularly IL-2 production. No significant differences were noted in either the production of rheumatoid factor or natural killer cell activity, irrespective of age or diet.
author Morrow, W J
Homsy, J
Swanson, C A
Ohashi, Y
Estes, J
Levy, J A
author_facet Morrow, W J
Homsy, J
Swanson, C A
Ohashi, Y
Estes, J
Levy, J A
author_sort Morrow, W J
title Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
title_short Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
title_full Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
title_fullStr Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
title_full_unstemmed Dietary fat influences the expression of autoimmune disease in MRL/lpr/lpr mice.
title_sort dietary fat influences the expression of autoimmune disease in mrl/lpr/lpr mice.
publishDate 1986
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1453202/
https://ncbi.nlm.nih.gov/pubmed/3491785
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