b-Cyclodextrin is a compound that forms inclusion complexes with a variety of molecules, specially bile acids and sterols. This study examines the effects of b-cyclodextrin on cholesterol and bile acid metabolism in hypercholesterolaemic rats. Male Wistar rats were divided into 4 groups that received during 7 weeks: control diet, 2% cholesterol diet (A), Aπ2.5% b-cyclodextrin (B) and Aπ5% b-cyclodextrin (C). The cholesterol-rich diet induced hepatomegaly and fatty liver and significantly reduced cholesterol, bile acid and phospholipid secretion. Addition of b-cyclodextrin normalised biliary lipid secretion. Moreover, when compared to A, b-cyclodextrin significantly lowered plasma phospholipid concentration (B: ª21%; C: ª29%) and the liver free/total cholesterol molar ratio (B: ª40%; C: ª38%), increased bile acid faecal output (B: π17%; C: π62%) and enhanced cholesterol 7a-hydroxylase activity (B:π50%; C: π100%) and mRNA levels (B: π14%; C: π29%). 5% b-cyclodextrin also reduced plasma triglycerides concentration (ª38%). However, ALT and AST activities were significantly increased (B: π140% and π280%; C: π72% and π135%) and there was a high incidence of cell necrosis with portal inflammatory cell infiltration. Addition of b-cyclodextrin to a cholesterol-rich diet results in a triglyceride-lowering action, enhancement of bile acid synthesis and excretion, and normalization of biliary lipid secretion, but produces a marked hepatotoxic effect.
Weight, plasma proteins, urinary accumulated creatinine, and nitrogen retention showed a better evolution in the group supplemented with the glutamine dipeptide when compared with the SPN group. Our results suggest a more suitable nutrition support in animals receiving L-alanyl-L-glutamine.
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