We previously reported that dietary stearic acid increased endogenous (biliary) cholesterol excretion in hamsters [Schneider et al, J. Nutr. 130:1232-1238, 2000]. To investigate the mechanisms responsible for this observation, we established a hypothesis that dietary stearic acid induces the gene expression of ATP binding cassette transporter G5 (ABCG5) and G8 (ABCG8) in the liver, consequently increasing biliary cholesterol secretion. To test this hypothesis, male Syrian hamsters (F1B hybrid) were fed a modified version of the NIH-07 open formula, cereal-based rodent diet enriched in one of the following 5 dietary fatty acids: palmitic acid (16:0), stearic acid (18:0), trans fatty acids (18:1t), oleic acid (18:1c), or linoleic acid (18:2). Hamsters fed 18:0 had significantly lower liver cholesterol concentrations compared with the other treatment groups and significantly lower plasma total cholesterol compared with hamsters fed 16:0 and 18:1t. Reverse transcriptase-polymerase chain reaction analysis showed that both ABCG5 and ABCG8 were expressed mainly in hamster liver and small intestine. Hepatic ABCG5 and ABCG8 mRNA levels, measured by RNase protection assay, showed hamsters fed 18:1t and 18:2 had significantly higher ABCG5 mRNA levels in liver compared with the other groups. Hepatic ABCG8 mRNA levels were significantly higher in 18:1t compared with 18:0 and 18:1c. These data indicate that the expression of ABCG5 and ABCG8 are responsive to specific dietary fatty acids, but that dietary 18:0 did not increase their expression as expected. Therefore, the increase in biliary cholesterol excretion by 18:0 as previously reported is most likely mediated by pathways independent of ABCG5 and ABCG8.
- Biliary cholesterol
- Stearic acid
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics