Abstract
1. 1. Other authors have suggested that bile salts may be the cholesterol metabolite responsible, in vivo, for the “feed-back” regulation of cholesterol synthesis in liver. 2. 2. Since the liver tumour lacks this feed-back control, the role of bile salts has been examined in 2 transplantable hepatomas-5123C in Buffalo rats and BW7756 in C57 L/J mice. 3. 3. This paper reports: first, that when bile salts were removed in vivo, by feeding the bile-salt adsorbent, cholestyramine, then cholesterol synthesis was increased in the liver but not in the hepatomas; secondly, that when a bile salt (sodium deoxycholate, 0.5 mM) was added in vitro, to an homogenate preparation, then cholesterol synthesis was inhibited in both liver and hepatoma; and thirdly, that when sodium deoxycholate was added to an incubation medium with tissue slices, then by contrast to the results with homogenates, cholesterol synthesis was inhibited in liver but not hepatoma. 4. 4. This is further evidence in support of the hypothesis that the defective control of lipid synthesis shown by hepatomas, which defect has been suggested as perhaps fundamental to the neoplastic process, may be due to an inability of metabolic regulators to reach the active sites of enzyme action.
Published Version
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