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. 2017 Dec 21;2(24):e96703. doi: 10.1172/jci.insight.96703

Figure 5. Deletion of ChREBP in the small intestine results in fructose intolerance.

Figure 5

(A) Western blot for carbohydrate responsive element–binding protein (ChREBP) in jejunal and liver whole-cell lysates of control (CTL) and intestine-specific ChREBP-KO (IChKO) mice. (B) Body weight and (C) food intake were measured in 6- to 8-week-old male and female control and IChKO mice fed high-fructose diet (HFrD) for 36 hours (n = 3 per group). (D) Eight-week-old female control and IChKO mice were fasted for 6 hours, and then gavaged with water or fructose and sacrificed 100 minutes later. Jejunal gene expression (n = 3 per group). (E) Representative images of small intestine and cecum in situ and (F) H&E–stained jejunal sections of control and IChKO after 36 hours of HFrD taken at ×10 magnification from mice described in B, as well as (G) serum TNF-α levels, (H) hepatic mRNA expression, and (I) serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity. Data are presented as box-and-whisker plots where the line in the box indicates the median, the box extends from the 25th to 75th percentiles, and the whiskers indicate the minimal and maximal values. P values were obtained using 2-way ANOVA. *P < 0.05 compared between water and fructose within the same genotype; #P < 0.05 compared between different genotypes within the same treatment group.