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Serologic and pathologic changes in rats on atherogenic diets

  • B.J. Neff
    Affiliations
    Department of Epidemiology, University of Michigan School of Public Health; Department of Pathology, University of Michigan Medical School, Ann Arbor, Mich. (U.S.A.)
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  • G.L. Brody
    Affiliations
    Department of Epidemiology, University of Michigan School of Public Health; Department of Pathology, University of Michigan Medical School, Ann Arbor, Mich. (U.S.A.)
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  • F.H. Epstein
    Affiliations
    Department of Epidemiology, University of Michigan School of Public Health; Department of Pathology, University of Michigan Medical School, Ann Arbor, Mich. (U.S.A.)
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  • T. Francis Jr.
    Affiliations
    Department of Epidemiology, University of Michigan School of Public Health; Department of Pathology, University of Michigan Medical School, Ann Arbor, Mich. (U.S.A.)
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      Summary

      Induction of experimental coronary atherosclerosis in rats was accompanied by the appearance in serum of a substance which inhibits the agglutination of chicken red cells by vaccinial hemagglutinin, a lipoprotein. Prolonged exposure to an “atherogenic diet” resulted in the development of elevated vaccinial hemagglutinin inhibitor (VHAI) titers. The animals in a second group maintained on a “high-fat diet” also frequently developed elevated VHAI titers as early as six weeks after being on the diet.
      A third control group of rats showed essentially no rise in inhibitor level. The appearance of VHAI may indicate a failure of physiologic competence to react to a stress such as an alteration in lipid metabolism. Possible relationships between vaccinial hemagglutinin and the lipoproteins involved in the pathogenesis of atherosclerosis are discussed.

      Résumé

      L'induction d'une athérosclérose coronarienne expérimentale chez le rat est associée à l'apparition dans le sérum d'une substance (une lipoprotéine) qui inhibe l'agglutination des globules rouges de poulet par une hemaglutinine vaccinale. La prolongation du régime athérogène provoque une augmentation du titre de cet inhibiteur (VHAI). Les animaux d'un second groupe maintenus à un régime riche en graisses ont fréquemment un titre élevé de VHAI dès 6 semaines après le début du régime. Le titre d'inhibiteur n'augmente pas dans un troisiènme groupe de rats témoins. L'apparition de VHAI traduit peut-être une altération des possibilités physiologiques de réaction à un stress tel qu'une altération du métabolisme des lipides. Les relations possibles entre l'hémaglutinine vaccinale et les lipoprotéines athérogènes sont discutées.

      Zusammenfassung

      Die experimentelle Entstehung einer coronaren Atherosklerose war bei Ratten von dem Auftreten einer Substanz im Serum begleitet, die die Agglutinierung von Hühnererythrocyten durch ein Haem-agglutinin des Vaccinevirus, einem Lipoproteid, hemmte. Bei Fortsetzung der “atherogenen Fütterung” stieg der Titer dieser die Haemagglutination hemmenden Substanz (VHAI) an. Auch die Tiere einer zweiten Versuchsserie, die fettreich ernährt wurden, entwickelten häufig bereits 6 Wochen nach Beginn der Diät erhöhnte VHAI-Titer. Eine dritte Kontrollgruppe zeigte im wesentlichen keinen Anstieg des Inhibitorspiegels. Das Auftreten der VHAI kann eine mangelhafte Fähigkeit des Organismus anzeigen, auf den Stress, den der Eingriff in den Lipidstoffwechsel darstellt, zu reagieren. Die m6glichen Beziehungen zwischen dem Haemagglutinin des Vaccinevirus and den Lipoproteiden, die in der Pathogenese der Atherosklerose eine Rolle spielen, werden erörtert.
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