(Cholesterol homeostasis in mammals is maintained through the coordinate regulation of three major metabolic pathways in the liver (Turley & Dietschy, 1982). Two pathways supply cholesterol to cells and include an endogenous biosynthetic pathway in which acetate is converted into cholesterol (Rilling & Chayet, 1985) and an exogenous pathway in which mem-bers of the low-density lipoprotein receptor family bind and internalize cholesterol-carrying particles from the blood (Hobbs et al., 1990). A third pathway is responsible for catabolism and involves the conversion of cholesterol into hydrophilic bile acids (Danielsson, 1973).

The mass of cholesterol fluxing through the human liver per day is large and minimally encompasses a biosynthetic output of 600 mg, a receptor-mediated uptake of 300 mg, a direct secretion component of 600 mg, and a bile acid synthesis component of 100-400 mg (Turley & Dietschy, 1982). Many proteins participate in cholesterol metabolism in the liver, including over 40 enzymes in the biosynthetic pathway (Rilling & Chayet, 1985), at least two endocytic receptors, a dozen or more bile acid biosynthetic enzymes, and numerous storage, transport, and regulatory proteins. The liver employsseveral strategies to coordinately regulate this cadre of proteins in an effort toprevent the pathological consequences of a disruption in overall cholesterol homeostasis. These tacts include shared negative feedback regulatory mechanisms at the transcriptional level (Goldstein & Brown, 1990) and physiological inter-twinings thatlink the activities of different key regulatory enzymes in each of the pathways. An example of this latter formof regulation is the Jekyll and Hyde roles that bile acids playin cholesterolhomeostasis.