Abstract:
: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.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Zou J,Chassaing B,Singh V,Pellizzon M,Ricci M,Fythe MD,Kumar MV,Gewirtz ATdoi
10.1016/j.chom.2017.11.003subject
Has Abstractpub_date
2018-01-10 00:00:00pages
41-53.e4issue
1eissn
1931-3128issn
1934-6069pii
S1931-3128(17)30497-3journal_volume
23pub_type
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