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. Author manuscript; available in PMC: 2011 Nov 5.
Published in final edited form as: Oncogene. 2011 Jan 10;30(18):2147–2160. doi: 10.1038/onc.2010.587

Figure 4.

Figure 4

Vhl inactivation blocks hepatic ketone production leading to decreased circulating ketone levels and death which is refractory to PPARα activation. (A) Levels of plasma ketones (acetoacetate plus 3-hydroxybutyrate) in animals fasted for 24 hours (for both genotypes, n = 2 for day 0, n = 4-8 for other time points). (B) Ketone body production by perfused livers isolated from 24 hours fasted animals at day 4 post Ad-Cre injection (n = 6 for each genotype); TK, total ketones; BHB, β-hydroxybutyrate; ACAC, acetoacetate. (C) In vitro fatty acid oxidation rates measured as 14CO2 production in liver homogenates from 24 hours fasted animals at day 3 post Ad-Cre injection (n = 2). (D) qRT-PCR analysis of PPARα target genes (or controls) normalized to Ppib in animals of the indicated genotypes 3 days after Ad-Cre injection and following 4 days of WY-14643 (WY), olive oil (vehicle), or no treatment (NT) (for both genotypes, n = 4-5 for each treatment). *, p value comparing VhlF/F vs. Vhl+/+; #, p value comparing WY to vehicle within the same mouse strain. (E) Survival curve for Ad-Cre injected animals treated with olive oil (vehicle) or WY-14643 (n = 5 for each genotype and treatment group). (F) Analysis of plasma triglycerides, same animals as in D (n = 3 per group). * and #, p < 0.05; ** and ##, p < 0.01.