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.
|Number of pages||1|
|Publication status||Published - 2015|
|Event||Keystone Symposia - Gut Microbiota Modulation of Host Physiology: The Search for Mechanism - Keystone, Colorado, United States|
Duration: 1 Mar 2015 → 6 Mar 2015
|Conference||Keystone Symposia - Gut Microbiota Modulation of Host Physiology: The Search for Mechanism|
|Period||01/03/2015 → 06/03/2015|