Fig. 3: Maternal high-fat diet disrupts offspring intestinal development via LRRC19. | Communications Biology

Fig. 3: Maternal high-fat diet disrupts offspring intestinal development via LRRC19.

From: Maternal high-fat diet disrupts intestinal mucus barrier of offspring by regulating gut immune receptor LRRC19

Fig. 3

A Experimental flow diagram of WT-MHFD and Lrrc19−/−-MHFD groups. Lrrc19+/− mice derived from the Lrrc19+/+ and Lrrc19−/− parents were crossbred to generate different genotypes of offspring, and the Lrrc19+/+ and Lrrc19−/− pups were selected for further analysis at 3 weeks old. The heterozygous Lrrc19+/− female mice were fed a high-fat diet during the period of gestation and lactation as described. B Genotype identification in the offspring of heterozygous mice. PCR of total DNA extracted from tail. +/+, wild-type mouse. +/–, heterozygous mouse. –/–, Lrrc19 knockout mouse. C Body weight of pups at 3 weeks of age in WT-MHFD and Lrrc19−/−-MHFD groups. n = 9 per group. D H&E staining of colonic tissues and colon crypts depth in the 3 weeks old offspring between WT-MHFD and Lrrc19−/−-MHFD groups. Five random fields from ×200 images were viewed for each mouse and the depth of well-orientated crypts was measured. Scale bar = 50 µm. n = 5 mice per group. E H&E staining of small intestinal tissues and the villus length of ileum in the 3-week-old offspring in WT-MHFD and Lrrc19−/−-MHFD groups. Five random fields from ×200 images were viewed for each mouse and the length of well-orientated villi was measured. n = 5 mice per group. MHFD, maternal high-fat diet. WT, wild type (Lrrc19+/+). Het, heterozygous type (Lrrc19+/−). ns, not significant. All data are displayed as means ± SDs. *p < 0.05.

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