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. 2022 Jan 19;13:386. doi: 10.1038/s41467-022-28044-x

Fig. 5. BHB selectively inhibited HDAC7 to preserve FOXO1 acetylation.

Fig. 5

a The distribution of HDAC4, HDAC5 and HDAC7 in the nucleus and cytoplasm of HADHA-overexpressed hepatocytes transfected with BDH1 siRNA with or without BHB (400 μM, 6 h) and 100 nM glucagon stimulation for 1 h (n = 3). b Immunoprecipitation analysis of interaction of FOXO1 with HDAC4, HDAC5 or HDAC7 in HADHA-overexpressed hepatocytes with or without BDH1 siRNA transfection. It was repeated 3 times independently with similar results. c Enzyme activity of HDAC4, HDAC5 and HDAC7 in HepG2 cells with 100 nM glucagon stimulation for 1 h after BHB treatment (400 μM, 6 h, n = 5). d Relative mRNA abundance of Pck1, G6pc and Pgc1a in HADHA-overexpressed hepatocytes transfected with BDH1 siRNA and HDAC7 siRNA (n = 6). e Immunoprecipitation analysis of FOXO1 acetylation in d. It was repeated 3 times independently with similar results. f Luciferase reporter assay of the effect of HADHA and HDAC7 on Pck1 and G6pc gene promoter. The Pck1 and G6pc luciferase reporters were co-transfected with HADHA, FOXO1 and HDAC7 plasmid in HEK-293T cells. The luciferase activity was normalized with the internal control (Renilla luciferase, n = 6). Values represent mean ± SEM. Statistical differences were determined by one-way ANOVA. Source data are provided as a Source Data file.