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Research Article| Volume 63, ISSUE 1, P147-157, January 1964

Dietary atherogenesis in alloxan diabetes

  • Norman Kalant
    Affiliations
    From the Research Laboratory and Hematology Laboratory, Jewish General Hospital, Department of Investigative Medicine, McGill University, Montreal, Quebec, Canada

    From the Department of Pathology University College of the West Indies Kingston, Jamaica
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  • Jacobo I. Teitelbaum
    Affiliations
    From the Research Laboratory and Hematology Laboratory, Jewish General Hospital, Department of Investigative Medicine, McGill University, Montreal, Quebec, Canada

    From the Department of Pathology University College of the West Indies Kingston, Jamaica
    Search for articles by this author
  • Arthur A. Cooperberg
    Affiliations
    From the Research Laboratory and Hematology Laboratory, Jewish General Hospital, Department of Investigative Medicine, McGill University, Montreal, Quebec, Canada

    From the Department of Pathology University College of the West Indies Kingston, Jamaica
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  • W.Arthur Harland
    Affiliations
    From the Research Laboratory and Hematology Laboratory, Jewish General Hospital, Department of Investigative Medicine, McGill University, Montreal, Quebec, Canada

    From the Department of Pathology University College of the West Indies Kingston, Jamaica
    Search for articles by this author
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      Abstract

      Normal and alloxan-diabetic rats were fed a high-fat diet. At intervals after starting the diet, animals from each group were killed for histologic examination of the heart and for measurement of plasma lipids and of certain coagulation factors. Both groups of animals showed increases in the plasma concentrations of factors II, V, VII, VIII, and X, decreases in the concentration of antithrombin and in prothrombin time, recalcification time, and Stypven time. The changes in the 2 groups were virtually identical in degree and time. The plasma concentrations of cholesterol, total phospholipids, and phosphatidyl ethanolamine rose in both groups but were higher in the diabetic animals. Athcromatous lesions developed more rapidly and were more extensive in the diabetic group. It is concluded that insulin deficiency in the rat increases susceptibility to atheroma formation associated with a high-fat diet, that this increase is not due to an increase in the hypercoagulable state beyond that produced in non-diabetic rats by such a diet, and that the clotting changes were not directly related to the plasma concentration of total phospholipids or of phosphatidyl ethanolamine.
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