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. Author manuscript; available in PMC: 2018 Jun 1.
Published in final edited form as: Endocr Relat Cancer. 2017 Mar 28;24(6):253–265. doi: 10.1530/ERC-16-0536

Figure 2.

Figure 2

Effect of Pten deletion in Lgr5+-ISCs and obesity on ISC proliferation and Akt signaling in intestine. (A) Mice fed a high fat diet gained significantly more body weight as compared to their low fat-fed counterparts (P<0.001) [Con LFD (n=8), Pten KO LFD (n=9), Con HFD (n=14), Pten KO HFD (n=17)]. Paraffin-embedded sections of small intestine from all 4 groups were immunostained for BrdU after a 24-hour pulse. (B) Two-way ANOVA in duodenum revealed a significant main effect for Pten KO (P<0.001) and diet (P<0.05), but no significant interaction. Similarly, a main effect for Pten KO was observed in jejunum (P<0.01) and ileum (P<0.001), but no effect of diet or its interaction was observed [Con LFD (n=7), Pten KO LFD (n=5), Con HFD (n=3), Pten KO HFD (n=6)](C) Two-way ANOVA for pAkt positive staining revealed a significant main effect for Pten KO only in duodenum (P=0.05), but no effect of diet or its interaction was observed on immunostaining for p-Akt positive cells. [Con LFD (n=7), Pten KO LFD (n=7), Con HFD (n=7), Pten KO HFD (n=7)]. Slides were scanned at 20× and histologic analysis was performed on 250 crypt-villi units in jejunum and ileum, and 100 crypt-villi units in duodenum, per sample in each independent experiment. Different letters denote a significant difference between groups, P<0.01.