The effects of cholesterol feeding on bile acid production in vitro in liver were contrasted with those in a strain of Morris hepatoma active in sterol synthesis. The principal conclusions are as follows:

Bile acid production de novo from acetate in liver is suppressible by dietary cholesterol in a fashion exactly comparable with, and related to, the cholesterol negative feedback phenomenon.

In liver, a dual, reciprocating precursor supply is available for bile acid formation. Dietary cholesterol, when present, functions in the presence of blockaded sterol synthesis, as the sole precursor of bile acid.

In the presence of a high-cholesterol diet, liver has the ability to convert mevalonate and stored dietary cholesterol simultaneously to bile acid.

Bile acid synthesis by a malignant tumor is described in this report. The tumor (Morris hepatoma 3924A) is active in bile acid production from both acetate and mevalonate, but these syntheses are totally unaffected by dietary cholesterol. Moreover, dietary cholesterol cannot itself be utilized by the tumor for bile acid synthesis.


This work was supported by USPHS Grants CA 11969-02, HL 14141, and CA 10729, Grant DRG 1120-2 from the Damon Runyon-Walter Winchell Memorial Cancer fund, and American Cancer Society Institutional Research Grant IN-51M.

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