Low esterified pectin protects from type 1 diabetes by reducing NLRP3 inflammasome activation, maintaining intestinal barrier integrity and by maintaining prediabetic microbiota compositions in NOD mice

[Speaker] Jia Sun:1
[Co-author] Chengfei Wu:1, Wenying Niu:1, Jiahong Li:1, Li-Long Pan:1
1:Laboratory of Immunopharmacology, School of Medicine, Jiangnan University, China

Accumulating evidence supports that the intestinal microbiota is involved in the pathogenesis of type 1 diabetes (T1D). Experimental therapeutic methods have been suggested to reserve the progression of T1D in animal models. However, limited successful therapies can be applied to human. Our aim was to evaluate whether long-term consumption of novel low esterified pectins dietary fibers can ameliorate T1D and explore the potential mechanisms. In non-obese diabetic mice, dietary intervention with pectins reduced the incidence of T1D. Pectins modified caecal microbiota, which produced more short-chain fatty acids especially acetate and butyrate, and regulated the regulatory T cell (Treg) generation and function. Furthermore, pectins improved the morphology of cecum, upregulating tight junction modulaory proteins, zonula occludens-2 and claudin-1 but not occludin and increasing the length of caecal villi. Additionally, pectins-supplemented mice were found to have less microbial antigens across the gut barrier and reduced inflammasome activation in the cecum and pancreas. Finally, lower-grade auto-inflammation was observed in the pancreas of pectins-supplemented mice. Our data demonstrated that this novel low esterified pectin, targeting caecal microbiota and cecum morphology, reduced the incidence of T1D and pectin supplementation may represent an effective nutritional intervention for the condition.

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