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.
Highlights
Obesity is associated with chronic low-grade inflammation
MOS showed a trend toward a decreased F4/80 expression mainly on high fat diet (HFD) (P = 0.066; Fig 2F; Table 2) which was likely due to an interaction with diet (LFD/HFD) (P = 0.086; Fig 2F; Table 2). These results showed that MOS supplementation has extra-intestinal immune modulatory properties by reducing M2-like monocytes on both diets and increasing eosinophils on low fat diet (LFD), whilst showing a trend toward reduced T cells on both diets and F4/80 expression on HFD in mesenteric white adipose tissue (mWAT)
We showed that MOS supplementation mildly altered immune cell composition in both mWAT and liver, which was not accompanied by ameliorations in HFD-induced
Summary
Obesity is associated with chronic low-grade inflammation. Obesity induces a phenotypic switch in the expanding white adipose tissue (WAT) from an anti-inflammatory towards a pro-inflammatory state which is characterized by an increase in M1-like macrophages, cytotoxic T cells, B cells, and neutrophils, whereas the numbers of M2-like macrophages, regulatory T cells, and eosinophils are reduced [1,2,3,4,5].WAT inflammation results in the release of pro-inflammatory cytokines and fatty acids in the circulation, which are key mediators in inducing insulin resistance and inflammation in other organs, including the liver [6]. Obesity induces a phenotypic switch in the expanding white adipose tissue (WAT) from an anti-inflammatory towards a pro-inflammatory state which is characterized by an increase in M1-like macrophages, cytotoxic T cells, B cells, and neutrophils, whereas the numbers of M2-like macrophages, regulatory T cells, and eosinophils are reduced [1,2,3,4,5]. MOS are derived from the outer cell-wall membrane of bacteria, plants, or yeast and have been shown to be resistant to hydrolysis by the action of digestive enzymes in the human gut [11]. They are widely used in the animal industry as food supplements to reduce pathogenic contamination and to improve economic performance [12,13]
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