Andersen, Daniel

Bahl, Martin Iain

Hansen, Axel Kornerup

Hansen, Camilla Hartmann Friis

Hellgren, Lars

Licht, Tine Rask

Pedersen, Susanne Brix

Zhang, Li

Dietary gluten and its component gliadin are well-known environmental triggers of celiac disease and important actors in type-1 diabetes, and are reported to induce alterations in the intestinal microbiota. However, research on the impact of gluten on type-2 diabetes in non-celiac subjects is more limited. The aim of this study was to investigate the effect of gliadin on glucose homeostasis and intestinal ecology in the mouse.Forty male C57BL/6 mice were fed a high-fat diet containing either 4% gliadin or no gliadin for 22 weeks. Gliadin consumption significantly increased the HbA1c level over time, with a borderline significance of higher HOMA-IR (homeostasis model assessment of insulin resistance) after 22 weeks. Sequencing of the V3 region of the bacterial 16S rRNA genes showed that gliadin altered the abundance of 81 bacterial taxa, separating the intestinal microbial profile of the gliadin consuming mice from the control mice in the principal coordinate analysis (PCoA) of weighted UniFrac distance. Moreover, gliadin reduced the ileal gene expression of tight junction protein 1, occludin, cadherin 1, mucin 2 and mucin 3, indicating an impaired intestinal barrier function. No difference was found in body weight gain, feed consumption or circulating cytokines (IL-1β, IL-6, IFN-γ, TNF-α and IL-10).Our study is the first to show that gliadin as part of a defined synthetic feed exacerbates the glycaemia and alters the intestinal microbiota composition. Comprehensive analyses of metabolites, histological sections and the profile of specific immune cells are in progress to elucidate the mechanism behind the observed effects.<br/

Online Research Database In Technology

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Gliadin affects glucose homeostasis and intestinal metagenome in C57BL6 mice fed a high-fat diet

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Gliadin affects glucose homeostasis and intestinal metagenome in C57BL6 mice fed a high-fat diet

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