Pregnancy impairs maternal intestinal barrier integrity in control and obese mice.
Thursday, February 13, 2020
4:15 PM – 4:30 PM
Location: Max Bell - MB253
Introduction: Obesity and metabolic dysfunction have been associated with the gut microbiota, however, this relationship in the context of pregnancy is still unclear. We have shown that obesity during pregnancy results in altered maternal gut microbial populations and induces maternal intestinal inflammation. Intestinal inflammation, barrier integrity, and metabolism are key inter-related factors that underpin microbial–host interactions, but whether maternal intestinal barrier integrity changes during pregnancy remains unknown. We aimed to determine the impact of pregnancy on maternal intestinal barrier integrity and whether intestinal barrier integrity changes in the context of maternal obesity.
Methods: C57BL/6J female mice were fed a control (17% kcal fat, CON) or a high fat diet (60% kcal fat, HFD) for 6 weeks prior to (non-pregnant, NP, cohort) and during pregnancy Intestinal barrier integrity was tested in both NP and pregnant mice at embryonic day (E) 14.5 (n=15 per group) using in vivo experimentation. All four groups of mice were gavaged with 80mg/kg fluorescently labelled-4kDa FITC-Dextran and blood samples were collected over 4 hours and fluorescence measured; the higher the values, the more permeable the intestine. Data were analyzed using a two-way ANOVA with Bonferroni post hoc.
Results: HFD-fed females gained significantly more weight than controls (p < 0.05). NP obese females had shorter small and large intestine length, and also caecal weight in no-pregnant and pregnant mice (p < 0.05). HFD-fed and CON-fed pregnant mice had increased intestinal permeability by 81% and 157% respectively as compared with NP control and NP HFD mice (p < 0.05). An obesogenic diet during pregnancy further increased intestinal permeability by 53% compared with Control pregnant mice at E14.5 (p < 0.05).
Conclusion: These data demonstrate that pregnancy impairs maternal intestinal barrier function, and maternal obesity exacerbates this intestinal adaptation.