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Experimental Atherosclerosis and Portacaval Shunt
FERDINAND F. McALLISTER, M.D.;
ROBERT BERTSCH, M.D.;
GERARD D'ALESSIO, B.S.
AMA Arch Surg. 1961;82(1):66-68.
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The role of the liver in cholesterol metabolism and experimental atherogenesis is not completely understood. Katz and Stamler1 in their familiar monograph on "Experimental Atherosclerosis" state that, to their knowledge, "no thorough-going studies have been carried out on the influence of hepatic factors on atherogenesis in experimental animals." According to the texts, free cholesterol exists in the blood stream as a result of the breakdown of erythrocytes and other cells and is excreted by the liver in bile—the only body fluid in which it is readily soluble. In addition, the liver may synthesize cholesterol from acetate by a process involving some 26 separate enzymatic reactions. According to Siperstein and Guest,2 exogenous cholesterol may exert some control over this synthesis by a feedback mechanism probably blocking the synthesis prior to the formation of squalene. Little else appears to be known of the handling of exogenous cholesterol by the liver.
. . . [Full Text PDF of this Article]
Author Affiliations
NEW YORK
From the Department of Surgery, Columbia University, College of Physicians and Surgeons.
Footnotes
Submitted for publication June 16, 1960.
Aided by Grants from the New York Heart Association and the United States Public Health Service.
Read before the Eighth Scientific Meeting of the International Cardiovascular Society, North American Chapter, Miami Beach, June 11, 1960.
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