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Research article2017Peer reviewed

Wholegrain oat diet changes the expression of genes associated with intestinal bile acid transport

Andersson, Kristina E.; Chawade, Aakash; Thuresson, Narda; Rascon, Ana; Oste, Rickard; Sterner, Olov; Olsson, Olof; Hellstrand, Per

Abstract

ScopeThe molecular mechanisms underlying the cholesterol-lowering properties of oats are only partly known. To study possible pathways involved, we investigated gene expressions in the liver and small intestine of mice fed oats.Method and resultsCholesterol and bile acids were analyzed in plasma and feces from LDL-receptor deficient (LDLr-/-) mice fed Western diet with wholegrain oats. A transcriptome analysis of mRNA from liver and jejunum was performed together with quantitative RT-PCR. Oat-fed mice had lower levels of plasma lipids and increased levels of bile acids and cholesterol in feces compared with controls. Two hundred thirty nine genes in jejunum and 25 genes in liver were differentially expressed (FDR corrected p < 0.05). The most affected biological process in jejunum was lipid biosynthesis and regulation. The apical sodium-dependent bile acid transporter (ASBT, Slc10a) and the intracellular bile acid binding protein (Fabp6) were both upregulated, whereas small heterodimer partner-1 (Shp-1) and apolipoprotein CII (Apoc2) were downregulated.ConclusionsWhole oats attenuated responses typically induced by high-fat diet. Increased expression of genes for intestinal bile acid uptake following oat consumption suggests retention in the gut lumen rather than decreased uptake capacity as cause for the increased bile acid excretion and the concomitant reduction of plasma cholesterol.

Keywords

Bile acids; Cholesterol; Diet; Gene expression; Oats

Published in

Molecular Nutrition and Food Research
2017, Volume: 61, number: 7, article number: 1600874

    UKÄ Subject classification

    Zoology
    Immunology
    Bioinformatics and Systems Biology

    Publication identifier

    DOI: https://doi.org/10.1002/mnfr.201600874

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/85398