In humans, the metabolic syndrome is associated with changes in the composition of the gut microbiota. Researchers hypothesize that diets rich in processed foods and low in dietary fibre disrupt the symbiotic relationship between the gut microbiota and the intestine. A disrupted host–microbiota relationship results in gut bacteria infiltrating the inner mucus layer, where they can interact with gut epithelial cells and promote inflammation.
Now, Andrew Gewirtz and colleagues have shown that a diet enriched with the fermentable fibre inulin can restore a healthy host–microbiota relationship in mice fed on a high-fat diet (HFD) and re-energize inner mucus layer defences.
Data from Gewirtz's group indicates that a harmonious relationship between the gut microbiota and the intestine promotes metabolic health. When the gut and intestine are in harmony, the gut bacteria reside in the outer mucus layer and the inner mucus layer is largely free from bacteria.
“A disturbance in this host–microbiota relationship, which can occur if the mucosal immune system is compromised or if the microbiota are antagonized with synthetic dietary emulsifiers, such as carboxymethyl cellulose and polysorbate 80, promotes low-grade inflammation that impairs metabolic signalling and promotes the metabolic syndrome,” explains Gewirtz. “In the present study, [we sought to investigate whether dietary fibre could promote a healthy] host–microbiota relationship and, consequently, prevent the metabolic syndrome.”
To uncover the role of dietary fibre in the host–microbiota relationship, Gewirtz and colleagues fed mice a HFD to simulate the metabolic syndrome. As HFDs are low in fibre, the authors supplemented the HFD with one of two types of fibre — cellulose or inulin. Cellulose is insoluble and not metabolized by mice, whereas inulin is readily metabolized by mice. The authors then studied the host–microbiota relationship and metabolism of the mice.
Gewirtz and colleagues found that the gut microbiota populations of mice fed on a HFD were reduced tenfold compared with the microbiota of mice fed a standard chow diet, a reduction that Gewirtz suggests could result in reduced host intestinal defences. In addition, the authors show that different species of bacteria in the gut respond differently to a HFD. Specifically, the species of bacteria that encroach upon intestinal epithelial cells and disrupt the host–microbiota relationship are enriched by a HFD, resulting in HFD-associated low-grade inflammation that promotes the metabolic syndrome.
“The authors found that the mechanism by which bacteria restore host defences is dependent on the cytokine IL-22”
Enrichment of the HFD with inulin, but not cellulose, resulted in the restoration of the gut bacteria that are beneficial to the host–microbiota relationship, and a boost to the intestinal defences. These inulin-associated changes to the gut microbiota prevented bacterial encroachment into the inner mucus layer and protected the mice from HFD-induced metabolic syndrome. The authors found that the mechanism by which bacteria restore host defences is dependent on the cytokine IL-22. Gewirtz's group are now trying to understand how a healthy population of gut bacteria restores IL-22 and how to optimize specific fibre types that would fully and safely restore a healthy microbiota.
“This study highlights the importance of consuming a diet rich in fermentable fibre, which is found in many fruits and some vegetables,” concludes Gewirtz. “In the future, it might be possible to engineer processed foods that promote a healthy microbiota and gut, and therefore metabolic health, but we do not believe the basic knowledge to do this safely is currently in hand.”
Zou, J. et al. Fiber-mediated nourishment of gut microbiota protects against diet-induced obesity by restoring IL-22-mediated colonic health. Cell Host Microbe http://dx.doi.org/10.1016/j.chom.2017.11.003 (2017)
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Morris, A. Fibre restores healthy gut microbiota. Nat Rev Endocrinol 14, 63 (2018). https://doi.org/10.1038/nrendo.2017.182
Scientific Reports (2019)