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. 2020 Sep 14;11(2):389–406. doi: 10.1016/j.jcmgh.2020.09.004

Figure 9.

Figure 9

L-PK silencing attenuates mitochondrial glucose oxidation. Metabolomic analyses of AML12 cells transfected with either scrRNA or siPklr and grown in media containing [U-13C6]-glucose and hepatic extracts from L-PK KD mice. (A) Abundance levels of alanine and citrate; (B) metabolite ratios of aspartate to glutamate in AML12 cells and their corresponding levels in liver extracts of L-PK KD mice. (C) Mole percent enrichment of labeled carbon into citrate, fumarate, and malate. (D) Enrichment of glucose-derived carbons into the M+3 isotopomers of pyruvate, lactate, and alanine in AML12 cells. (E) Schematic of changes in pyruvate flux into TCA cycle using (U)13C glucose tracing in AML12 cells. ALT, alanine aminotransferase; AsAT, aspartate aminotransferase; GLS, glutaminase; KD, knockdown; LDH, lactate dehydrogenase; ME, malic enzyme; MPC, mitochondrial pyruvate carrier; PC, pyruvate carboxylase; PDH, pyruvate dehydrogenase. Data are presented as mean ± SEM (n = 3 cells or 5 livers per group). ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 by t test.