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Dietary α-cyclodextrin reduces atherosclerosis and modifies gut flora in apolipoprotein E-deficient mice.

Authors :
Sakurai T
Sakurai A
Chen Y
Vaisman BL
Amar MJ
Pryor M
Thacker SG
Zhang X
Wang X
Zhang Y
Zhu J
Yang ZH
Freeman LA
Remaley AT
Source :
Molecular nutrition & food research [Mol Nutr Food Res] 2017 Aug; Vol. 61 (8). Date of Electronic Publication: 2017 Feb 24.
Publication Year :
2017

Abstract

Scope: α-Cyclodextrin (α-CD), a cyclic polymer of glucose, has been shown to lower plasma cholesterol in animals and humans; however, its effect on atherosclerosis has not been previously described.<br />Methods and Results: apoE-knockout mice were fed either low-fat diet (LFD; 5.2% fat, w/w), or Western high fat diet (21.2% fat) containing either no additions (WD), 1.5% α-CD (WDA); 1.5% β-CD (WDB); or 1.5% oligofructose-enriched inulin (WDI). Although plasma lipids were similar after 11 weeks on the WD vs. WDA diets, aortic atherosclerotic lesions were 65% less in mice on WDA compared to WD (P < 0.05), and similar to mice fed the LFD. No effect on atherosclerosis was observed for the other WD supplemented diets. By RNA-seq analysis of 16S rRNA, addition of α-CD to the WD resulted in significantly decreased cecal bacterial counts in genera Clostridium and Turicibacterium, and significantly increased Dehalobacteriaceae. At family level, Comamonadaceae significantly increased and Peptostreptococcaceae showed a negative trend. Several of these bacterial count changes correlated negatively with % atherosclerotic lesion and were associated with increased cecum weight and decreased plasma cholesterol levels.<br />Conclusion: Addition of α-CD to the diet of apoE-knockout mice decreases atherosclerosis and is associated with changes in the gut flora.<br /> (© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Details

Language :
English
ISSN :
1613-4133
Volume :
61
Issue :
8
Database :
MEDLINE
Journal :
Molecular nutrition & food research
Publication Type :
Academic Journal
Accession number :
28102587
Full Text :
https://doi.org/10.1002/mnfr.201600804