Cholesterol-sequestering agent

Angelin et al. reported recently that treatment with a bile-salt-sequestering agent reduced the postprandial but not the fasting serum bile acid levels in human [219]. It was concluded that the postprandial bile acid inflow to the liver may be more important as a regulator of bile acid biosynthesis than the fasting level of bile acids, supporting the contention that a certain concentration of bile acids must be reached in the portal blood to obtain an efficient inhibition of the cholesterol 7a-hydroxyl-ase. 

As discussed earlier (see Section VB2), cholestyramine is an unabsorb-able bile acid sequestering agent which reduces serum cholesterol by markedly augmenting fecal elimination of bile acids in both normo- and hypercho-lesterolemic patients (Fig. 3 11,90,94,153,154,283,284). 

Beher et al. (23,24) concluded that pituitary hormones act on sterol and bile acid elimination rather than on bile acid synthesis. They supported this argument by studies using cholestyramine (23,26), a bile acid sequestering anion exchanger, and psyllium hydrocolloid (27), which provides dietary bulk and lowers tissue cholesterol. Both of these agents decreased the /1/2 and increased the synthesis and excretion of the bile acids in hypophysectomized rats but did not affect bile acid pool size. Thus the faster bile acid synthesis and excretion rates in MK-135 [cholestyramine] treated animals are due to an increased rate of elimination of bile acids from their pools. Since bile acid pool size did not change in the hypophysectomized rats, they concluded that the defect in sterol metabolism in these animals [hypophysectomized] is concerned not with the conversion of liver sterols to bile acids but with the rate of elimination of bile acids from their pools. (23)... 

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