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Experimental Atherosclerosis and Portacaval Shunt

Arch Surg. 1961;82(1):66-68. doi:10.1001/archsurg.1961.01300070070009.
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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.


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