Premium
Dietary Mannan Oligosaccharides Modulate Gut Microbiota, Increase Fecal Bile Acid Excretion, and Decrease Plasma Cholesterol and Atherosclerosis Development
Author(s) -
Hoving Lisa R.,
Katiraei Saeed,
Heijink Marieke,
Pronk Amanda,
der WeePals Lianne,
Streefland Trea,
Giera Martin,
Willems van Dijk Ko,
Harmelen Vanessa
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700942
Subject(s) - gut flora , cholesterol , bacteroides , hyperlipidemia , butyrate , excretion , inflammation , cecum , endocrinology , feces , medicine , lipoprotein , biology , chemistry , biochemistry , microbiology and biotechnology , bacteria , genetics , fermentation , diabetes mellitus
Scope Mannan oligosaccharides (MOS) have proven effective at improving growth performance, while also reducing hyperlipidemia and inflammation. As atherosclerosis is accelerated both by hyperlipidemia and inflammation, we aim to determine the effect of dietary MOS on atherosclerosis development in hyperlipidemic ApoE*3‐Leiden.CETP ( E3L.CETP ) mice, a well‐established model for human‐like lipoprotein metabolism. Methods and results Female E3L.CETP mice were fed a high‐cholesterol diet, with or without 1% MOS for 14 weeks. MOS substantially decreased atherosclerotic lesions up to 54%, as assessed in the valve area of the aortic root. In blood, IL‐1RA, monocyte subtypes, lipids, and bile acids (BAs) were not affected by MOS. Gut microbiota composition was determined using 16S rRNA gene sequencing and MOS increased the abundance of cecal Bacteroides ovatus . MOS did not affect fecal excretion of cholesterol, but increased fecal BAs as well as butyrate in cecum as determined by gas chromatography mass spectrometry. Conclusion MOS decreased the onset of atherosclerosis development via lowering of plasma cholesterol levels. These effects were accompanied by increased cecal butyrate and fecal excretion of BAs, presumably mediated via interactions of MOS with the gut microbiota.