Impact of beta-cyclodextrin and resistant starch on bile acid metabolism and fecal steroid excretion in regard to their hypolipidemic action in hamsters

To examine the impact on bile acid metabolism and fecal steroid excretion a s a mechanism involved in the lipid-lowering action of beta-cyclodextrin an d resistant starch in comparison to cholestyramine, male golden Syrian hams ters were fed 0% (control), 8% or 12% of beta-cyclodextrin or resistant sta rch or 1% cholestyramine. Resistant starch, beta-cyclodextrin and cholestyr amine significantly lowered plasma total cholesterol and triacylglycerol co ncentrations compared to control. Distinct changes in the bile acid profile of gallbladder bile were caused by resistant starch, beta-cyclodextrin and cholestyramine. While cholestyramine significantly reduced chenodeoxychola te independently of its taurine-glycine conjugation, beta-cyclodextrin and resistant starch decreased especially the percentage of taurochenodeoxychol ate by -75% and -44%, respectively. As a result, the cholate: chenodeoxycho late ratio was significantly increased by 100% with beta-cydodextrin and by 550% with cholestyramine while resistant starch revealed no effect on this ratio. beta-Cyclodextrin and resistant starch, not cholestyramine, signifi cantly increased the glycine:taurine conjugation ratio demonstrating the pr edominance of glycine conjugated bile acids. Daily fecal excretion of bile acids was 4-times higher with 8% beta-cyclodextrin and 19-times with 1% cho lestyramine compared to control. beta-Cyclodextrin and cholestyramine also induced a 2-fold increase in fecal neutral sterol excretion, demonstrating the sterol binding capacity of these two compounds. Resistant starch had on ly a modest effect on fecal bile acid excretion (80% increase) and no effec t on excretion of neutral sterols, suggesting a weak interaction with intes tinal steroid absorption. These data demonstrate the lipid-lowering potenti al of beta-cyclodextrin and resistant starch. An impaired reabsorption of c irculating bile acids and intestinal cholesterol absorption leading to an i ncrease in fecal bile acid and neutral sterol excretion is most likely the primary mechanism responsible for the lipid-lowering action of beta-cyclode xtrin. In contrast, other mechanisms involving the alterations in the bilia ry bile acid profile or repressed hepatic lipogenesis, e.g., VLDL productio n, appear to be involved in the hypolipidemic effect of resistant starch. ( C) 1999 Elsevier Science B.V. All rights reserved.