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. Author manuscript; available in PMC: 2018 Sep 5.
Published in final edited form as: Cell Metab. 2017 Sep 5;26(3):547–557.e8. doi: 10.1016/j.cmet.2017.08.004

Figure 3.

Figure 3

KD activates PPARα gene expression pattern distinct from HF. A, Experimental timeline. B–G, RNAseq transcriptome analysis of 1 week on diets in 12 mo old mice. B, Plasma BHB levels for study of immediate diet effects. C–D, Gene expression changes in liver, defined permissively for subsequent pathway analysis (Log2FC>0.38, P<0.02), show many genes down-regulated in common by KD and HF but few genes up-regulated in common. E–G, Top ingenuity upstream regulators associated with KD in liver (E), with the same regulators highlighted for HF in liver (F) and KD in kidney (G). PPARα activation pattern is present in both liver and kidney for KD, and not for HF. H–I, Study of 26 mo old Cyclic KD and Control mice. H, Q-PCR of genes involved in fatty acid synthesis, glucose/insulin signaling, and TOR activity. I, Q-PCR of PPARα target genes. B–G, 12 mo mice on diets for 1 week, collected at night, N = 5 Control, 7 KD, 6 HF. H–I, 26 mo mice on diets for 14 mo, collected at night during control-fed week, N = 8 Control, 8 Cyclic KD. See also Figure S4.