Extended Data Fig. 1: Intestine-specific Khk-C ablation increases fructose spillover to the colonic microbiota.
From: The small intestine shields the liver from fructose-induced steatosis
a, Khk-C floxed mice were generated by inserting two loxP sequences (black arrowheads) on both sides of a Khk-C specific exon (orange). The mice were then crossed with the Villin-Cre mice to generate intestine-specific Khk-C KO mice. b, qPCR (left) and western blots (right) show ablation of Khk-C in the jejunum but not in the liver (N = 6 mice for WT, 4 mice for KO). c, Khk-A mRNA is induced in the jejunum of KO mice (N = 6 mice for WT, 4 mice for KO). d, e, Mice received 1:1 mixture of 13C-fructose and unlabeled glucose (1 g/kg each) via oral gavage and the labeled F1P in duodenum and jejunum were measured in d and e, respectively (N = 3 mice for each time point). The AUC is shown on the right for the jejunum in e. f, AUC of labeled fructose in the cecal content over 1 h after gavage (N = 3 mice per group). g, Concentrations of total labeled carbons in acetate, propionate and butyrate in the cecal content 1 h or 2 h after gavage (N = 4, 3, 5, 5 mice). Data are mean ± standard error. Numbers in graphs indicate P-values by two-sided Student’s t-test.
