Fig. 3: Lkb1KOlivad (KO) mice have high levels of liver gluconeogenesis and enriched hepatic amino acid catabolism. | Nature Communications

Fig. 3: Lkb1KOlivad (KO) mice have high levels of liver gluconeogenesis and enriched hepatic amino acid catabolism.

From: Lkb1 suppresses amino acid-driven gluconeogenesis in the liver

Fig. 3

a Pyruvate tolerance test (PTT) (KO: n = 4, WT: n = 6). The area under the curve (AUC) of blood glucose level is shown. Data are presented as mean values ± SD. P values were determined by unpaired two-tailed t-test. ***p ≤ 0.001. b RT-qPCR analysis of the expression of Foxo-1 target genes in fasted mice (KO: n = 10, WT: n = 6). Data are presented as mean values ± SD. P values were determined by unpaired two-tailed t-test. ns: not significant; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001. c, d IPA analysis of the liver proteome of Lkb1KOlivad mice, showing the top-ranking enriched canonical pathways. The LFQ liver proteome analysis was done 15 days after tamoxifen injection on Lkb1KOlivad and control mice. The p value for pathway enrichment was obtained in right-tailed Fisher’s exact tests. The threshold for −log10(p value) determines the probability of each biofunction being assigned to the dataset and the canonical pathway not being due to chance alone. e Scheme of the amino acid catabolic pathways for gluconeogenesis and the urea cycle. The proteins for which enrichment was noted in the livers of mutant mice are shown in red. f Heatmap showing the enrichment in proteins involved in amino acid catabolism, amino acid uptake and the urea cycle in both the fasted and refed states. This heatmap was generated with Genesis clustering software. Proteins not upregulated are shown in gray. Source data are provided as a Source data file.

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