Extended Data Fig. 7: Intestine-specific Khk-C overexpression increases intestinal fructose catabolism.
From: The small intestine shields the liver from fructose-induced steatosis
a, Khk-C inducible overexpressing transgenic (TG) mice were generated by cloning a Khk-C coding sequence (orange) under the TET-on promoter (green). Then, the mice were crossed with mice that harbored Villin-Cre driver (blue) and rtTA with a stop-codon (gray) in the ROSA26 genomic region. Mice were fed with doxycycline in the drinking water to induce deletion of the stop-codon and subsequent Khk-C overexpression in the Villin-expressing intestinal epithelial cells. b, qPCR (left) and western blots (right) show Khk-C induction in the jejunum but not in the liver (N = 4 mice per group). The exposure time for Khk-C blot in the jejunum was decreased to prevent signal saturation. c, Khk-A mRNA levels were measured in the liver or jejunum (N = 4 mice per group). d, e, Mice received 1:1 mixture of 13C-fructose and unlabeled glucose (1 g/kg each) via oral gavage and the levels of labeled F1P and glycerate in the jejunum were measured in d, e, respectively (N = 3 mice for each time point). AUC is shown on the right. Data are mean ± standard error. Numbers in graphs indicate P-values by two-sided Student’s t-test.
