Extended Data Fig. 5: Intestinal AMPKα1 deficiency improves NASH via decreasing ceramide generation.
From: Gut bacteria alleviate smoking-related NASH by degrading gut nicotine
Eight-week-old male Prkaa1fl/fl and Prkaa1ΔIE mice were administered a HFHCD plus nicotine water for 20 weeks (SPF, n = 8 mice/group). a, Liver weight. b–e, Serum TG (b), hepatic CE (c), serum CE (d) and serum NEFA (e) contents. f–j, Histology scores of hepatic steatosis (f), lobular inflammation (g), ballooning (h), NAFLD activity (i), and fibrosis stage (j). k-m, Relative mRNA levels of genes related to hepatic lipid metabolism (k), inflammation (l) and fibrosis (m). n, o, Eight-week-old male Prkaa1fl/fl (WT) and Prkaa1ΔIE (KO) mice were administered a HFHCD plus nicotine water for 20 weeks (SPF, Prkaa1fl/fl, n = 12 mice; Prkaa1ΔIE, n = 11 mice). PLS-DA analysis of lipid metabolites in the ileum (n). Random forest analysis showing the top 10 lipid metabolites that lead to differences in the ileal lipid profiles (o). p, A schematic diagram illustrating the workflow of phosphorylated proteomics. Created with BioRender. q, Volcano map of phosphorylated proteomics analysis from ileal epithelia of Prkaa1fl/fl (WT) and Prkaa1ΔIE (KO) mice (n = 5 mice/group) administered a HFHCD plus nicotine water for 20 weeks. Relative fold change (log2) of phosphorylated sites abundance was determined by comparing KO versus WT, and P values (–log10) were calculated by two-tailed t-test. Data are the means ± s.e.m. a–e, Two-tailed Student’s t-test. f–m, Two-tailed Mann- Whitney U-test.