Defective <i>Atg16l1</i> in intestinal epithelial cells links to altered fecal microbiota and metabolic shifts during pregnancy in mice.

A nonsignificant trend was observed for L-Fucose in Atg16l1 Δ IEC compared to Atg16l1 fl/fl pregnant mice ( Figure 5a,5c , p = 0.488).

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Although no formally significant differences were observed between Atg16l1 fl/fl and Atg16l1 ∆IEC mice at week 3 at the genus level, we observed a clear trend toward a decrease in Lachnospiracea NK4A136 group , Lachnospiraceae UCG-001 , Lachnoclostridium , Lactobacillus , and Roseburia in Atg16l1 ∆IEC mice ( Figure 4d , Supplementary Figure S5A) that recapitulates the findings in Figure 1d .

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89 Metabolomic profiling only revealed a suggestive trend of fecal L-Fucose in Atg16l1 ∆IEC mice at trimester 3, which may warrant further investigation due to the important role of fucosylation as a post-translational protein modification in Crohn’s disease and colorectal cancer. 26 , 90–92 We found consistent evidence for an increase in chitin-degradation in Atg16l1 ∆IEC pregnant mice in trimester 3 (day 18 after timed mating), both by higher abundance of the pathway in metagenomic data, as well as increased levels of its metabolite N-acetylglucosamine in the feces of these mice.

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