Fig. 7

Intestine-specific RORA deficiency mimics or worsens maternal diabetes-mediated gastrointestinal dysfunction. Dams from either the control (CTL) or diabetes (STZ) groups were crossbred with either wild type (WT) or intestinal epithelial-specific RORA knockout (RORA^−/−), and the gastrointestinal function of male offspring was evaluated. a–d The IEC cells were isolated to evaluate cytokine secretion, n = 9; a IL-1β secretion; b IL-6 secretion; c MCP1 secretion; d IL17A secretion. e Intestinal permeability assay by FITC-dextran, n = 5. f–j Gut microbiota analysis, n = 9; f overview of the identified relative frequencies of different phyla found in treated mice; g species richness; h species diversity; i relative abundance of Mucispirillumn at genus level; j relative abundance of different bacteria in phylum level. The two-way ANOVA analysis was performed to determine statistical significance of different groups. ***P < 0.0001; **P < 0.001; *P < 0.01; N/S, no significance. Data were expressed as mean ± SD