Back to Search Start Over

Dietary yeast-derived mannan oligosaccharides have immune-modulatory properties but do not improve high fat diet-induced obesity and glucose intolerance.

Authors :
Hoving, Lisa R.
van der Zande, Hendrik J. P.
Pronk, Amanda
Guigas, Bruno
Willems van Dijk, Ko
van Harmelen, Vanessa
Source :
PLoS ONE; 5/3/2018, Vol. 13 Issue 5, p1-17, 17p
Publication Year :
2018

Abstract

The indigestible mannan oligosaccharides (MOS) derived from the outer cell wall of yeast Saccharomyces cerevisiae have shown potential to reduce inflammation. Since inflammation is one of the underlying mechanisms involved in the development of obesity-associated metabolic dysfunctions, we aimed to determine the effect of dietary supplementation with MOS on inflammation and metabolic homeostasis in lean and diet-induced obese mice. Male C57BL/6 mice were fed either a low fat diet (LFD) or a high fat diet (HFD) with, respectively, 10% or 45% energy derived from lard fat, with or without 1% MOS for 17 weeks. Body weight and composition were measured throughout the study. After 12 weeks of intervention, whole-body glucose tolerance was assessed and in week 17 immune cell composition was determined in mesenteric white adipose tissue (mWAT) and liver by flow cytometry and RT-qPCR. In LFD-fed mice, MOS supplementation induced a significant increase in the abundance of macrophages and eosinophils in mWAT. A similar trend was observed in hepatic macrophages. Although HFD feeding induced a classical shift from the anti-inflammatory M2-like macrophages towards the pro-inflammatory M1-like macrophages in both mWAT and liver from control mice, MOS supplementation had no effect on this obesity-driven immune response. Finally, MOS supplementation did not improve whole-body glucose homeostasis in both lean and obese mice.Altogether, our data showed that MOS had extra-intestinal immune modulatory properties in mWAT and liver. However these effects were not substantial enough to significantly ameliorate HFD-induced glucose intolerance or inflammation. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
19326203
Volume :
13
Issue :
5
Database :
Complementary Index
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
129415634
Full Text :
https://doi.org/10.1371/journal.pone.0196165