Fig. 5: ACOT12 deficiency results in cholesterol accumulation via stimulation of PPARα.
From: Loss of Acot12 contributes to NAFLD independent of lipolysis of adipose tissue
a KEGG pathway analysis of RNA sequencing data of HFD Acot12−/− livers compared with Acot12+/+ livers. b Gene set analysis of RNA sequencing data of HFD Acot12−/− livers. c Immunostaining of PPARα in 8-week HFD-fed Acot12+/+ and Acot12−/− livers. The magnified image shows representative PPARα-positive sites in HFD-fed Acot12+/+ and Acot12−/− mouse livers. Scale bars, 200 μm. d Gene set analysis of human liver biopsy of a normal, NASH, steatosis patient-related GEO dataset (GSE48452). e Representative image of immunohistochemical staining of PPARα in liver biopsies from patients with steatosis with high ACOT12 expression (n = 18) and patients with steatosis with low ACOT12 expression (n = 18). f Histological score of immunohistochemical staining of ACOT12 and PPARα in liver biopsies of steatosis patients. High and low expression of ACOT12 sorted by H-score of 200. g Levels of TG and TC in Acot12+/+ and Acot12−/− mouse primary hepatocytes with or without acetate. h Transcription level of Ppara in Acot12+/+ and Acot12−/− mouse primary hepatocytes with or without acetate. i Expression level of lipogenesis genes in Acot12+/+ and Acot12−/− mouse primary hepatocytes with or without acetate. All data are presented as the mean ± SEM. Statistical differences between two groups were determined using unpaired two-tailed Student’s t test (f); statistical differences among four groups were performed using one-way ANOVA, followed by the Holm–Sidak multiple comparison test (g, h); statistical differences in individual gene expression among four groups were performed using two-way ANOVA, followed by Tukey’s multiple comparison test (i). n.s. nonsignificant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
