TY - JOUR
T1 - Fiber-Mediated Nourishment of Gut Microbiota Protects against Diet-Induced Obesity by Restoring IL-22-Mediated Colonic Health
AU - Zou, Jun
AU - Chassaing, Benoit
AU - Singh, Vishal
AU - Pellizzon, Michael
AU - Ricci, Matthew
AU - Fythe, Michael D.
AU - Kumar, Matam Vijay
AU - Gewirtz, Andrew T.
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2018/1/10
Y1 - 2018/1/10
N2 - Dietary supplementation with fermentable fiber suppresses adiposity and the associated parameters of metabolic syndrome. Microbiota-generated fiber-derived short-chain fatty acids (SCFAs) and free fatty acid receptors including GPR43 are thought to mediate these effects. We find that while fermentable (inulin), but not insoluble (cellulose), fiber markedly protected mice against high-fat diet (HFD)-induced metabolic syndrome, the effect was not significantly impaired by either inhibiting SCFA production or genetic ablation of GPR43. Rather, HFD decimates gut microbiota, resulting in loss of enterocyte proliferation, leading to microbiota encroachment, low-grade inflammation (LGI), and metabolic syndrome. Enriching HFD with inulin restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferation, and antimicrobial gene expression in a microbiota-dependent manner, as assessed by antibiotic and germ-free approaches. Inulin-induced IL-22 expression, which required innate lymphoid cells, prevented microbiota encroachment and protected against LGI and metabolic syndrome. Thus, fermentable fiber protects against metabolic syndrome by nourishing microbiota to restore IL-22-mediated enterocyte function. Dietary fiber supplements suppress adiposity and the associated parameters of metabolic syndrome. Zou et al. show that the fermentable fiber inulin impacts gut microbiota to increase intestinal epithelial proliferation, prevent colonic atrophy, reduce microbiota encroachment into the mucosa, and thereby protect against metabolic syndrome in a microbiota- and IL-22-dependent manner.
AB - Dietary supplementation with fermentable fiber suppresses adiposity and the associated parameters of metabolic syndrome. Microbiota-generated fiber-derived short-chain fatty acids (SCFAs) and free fatty acid receptors including GPR43 are thought to mediate these effects. We find that while fermentable (inulin), but not insoluble (cellulose), fiber markedly protected mice against high-fat diet (HFD)-induced metabolic syndrome, the effect was not significantly impaired by either inhibiting SCFA production or genetic ablation of GPR43. Rather, HFD decimates gut microbiota, resulting in loss of enterocyte proliferation, leading to microbiota encroachment, low-grade inflammation (LGI), and metabolic syndrome. Enriching HFD with inulin restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferation, and antimicrobial gene expression in a microbiota-dependent manner, as assessed by antibiotic and germ-free approaches. Inulin-induced IL-22 expression, which required innate lymphoid cells, prevented microbiota encroachment and protected against LGI and metabolic syndrome. Thus, fermentable fiber protects against metabolic syndrome by nourishing microbiota to restore IL-22-mediated enterocyte function. Dietary fiber supplements suppress adiposity and the associated parameters of metabolic syndrome. Zou et al. show that the fermentable fiber inulin impacts gut microbiota to increase intestinal epithelial proliferation, prevent colonic atrophy, reduce microbiota encroachment into the mucosa, and thereby protect against metabolic syndrome in a microbiota- and IL-22-dependent manner.
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U2 - 10.1016/j.chom.2017.11.003
DO - 10.1016/j.chom.2017.11.003
M3 - Article
C2 - 29276170
AN - SCOPUS:85038876729
SN - 1931-3128
VL - 23
SP - 41-53.e4
JO - Cell Host and Microbe
JF - Cell Host and Microbe
IS - 1
ER -