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Publication : Reduction of cholesterol absorption by dietary plant sterols and stanols in mice is independent of the Abcg5/8 transporter.

First Author  Plösch T Year  2006
Journal  J Nutr Volume  136
Issue  8 Pages  2135-40
PubMed ID  16857831 Mgi Jnum  J:114929
Mgi Id  MGI:3690410 Doi  10.1093/jn/136.8.2135
Citation  Plosch T, et al. (2006) Reduction of cholesterol absorption by dietary plant sterols and stanols in mice is independent of the Abcg5/8 transporter. J Nutr 136(8):2135-40
abstractText  Dietary supplementation with plant sterols, stanols, and their esters reduces intestinal cholesterol absorption, thus lowering plasma LDL cholesterol concentration in humans. It was suggested that these beneficial effects are attributable in part to induction of genes involved in intestinal cholesterol transport, e.g., Abcg5 and Abcg8, via the liver X receptor (LXR), but direct proof is lacking. Male C57BL/6J mice were fed a purified diet (control), diets containing cholesterol (0.12 g/100 g) only, or in combination with either plant sterols or stanols (0.5 g/100 g) for 4 wk. Plant sterols and stanols dramatically increased neutral fecal sterol excretion (2.2 and 1.4-fold, respectively, compared with cholesterol-fed mice; P < 0.05). Cholesterol and cholesterol ester concentrations were higher in livers of mice fed cholesterol compared with controls (+135% and +925%; P < 0.05). Plant sterols and stanols completely prevented cholesterol accumulation as well as induction of LXR target genes in liver. Feeding plant sterols and stanols did not alter intestinal expression of Abcg5, Abcg8, or other LXR target genes nor of Npc1l1. Fractional cholesterol absorption in Abcg5-/- mice was reduced to the same extent by dietary plant sterols (49%) as in wild-type littermates (44%). Plant sterol and stanol-induced reduction of cholesterol absorption in mice is not associated with upregulation of intestinal LXR target genes nor is it influenced by Abcg5-deficiency. Our data indicate that dietary plant sterols and stanols inhibit cholesterol absorption within the intestinal lumen independently of LXR.
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