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. 2023 May 2;12:e83353. doi: 10.7554/eLife.83353

Figure 3. Empagliflozin inhibits the utilization of pyruvate as a metabolic substrate in Alport syndrome (AS) podocytes.

(A, B) Bar graph analysis of endogenous and substrate-driven oxygen consumption rates in wild-type (WT) and Alport (AS) tubular cells (A) and podocytes (B) treated with or without empagliflozin (E) (n=3). The sequential addition of permeabilizing agent and substrates was labeled in the figure. (C) Pyruvate dehydrogenase (PDH) activity was measured by a colorimetric assay in protein extracts from AS podocytes, normalized to protein concentration (n=3). Two-tailed Student’s t-test, *p<0.5. FA: octanoylcarnitine; ML: malate-low concentration; MH: malate-high concentration; P: pyruvate; G: glutamate.

Figure 3.

Figure 3—figure supplement 1. Empagliflozin inhibits NADH-linked oxygen consumption rate in Alport syndrome (AS) podocytes.

Figure 3—figure supplement 1.

(A, B) Bar graph analysis of endogenous and substrate-driven oxygen consumption rates in wild-type (WT) and Alport (AS) tubular cells (A) and podocytes (B) treated with or without empagliflozin (E) (n=3). The sequential addition of permeabilizing agent and substrates was labeled in the figure. (C) Bar graph analysis of the relative rate of extracellular acidification in AS podocyte after empagliflozin treatment (n=3). Two-tailed Student’s t-test, *p<0.5, ***p< 0.001. MH: malate-high concentration; P: pyruvate; G: glutamate.