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. 2021 Oct 22;6(20):e142464. doi: 10.1172/jci.insight.142464

Figure 3. Bsg deficiency impairs hepatic availability of lactate and pyruvate in vivo.

Figure 3

(A) Schematic illustrating impaired gluconeogenesis resulting from decreased substrate import due to Bsg deficiency. OAA, oxaloacetate. (B) Blood glucose levels in Bsg+/+ and Bsg–/– mice under fasting conditions. White columns and circles, Bsg+/+ mice; gray columns and black circles, Bsg–/– mice (n = 10–12/genotype). Scatter plots display the data for individual mice. (C) Differences in blood lactate values between feeding and fasting states in Bsg+/+ or Bsg–/– female mice (n = 5–6/genotype). (D) Differences in serum pyruvate values between feeding and fasting states in Bsg+/+ or Bsg–/– female mice (n = 5–6/genotype). (E) G6P and F6P with incorporation of 13C3-labeled carbon in isolated Bsg+/+ or Bsg–/– hepatocytes. White columns, Bsg+/+ hepatocytes; gray columns, Bsg–/– hepatocytes. n = 5 for independent experiments. N.D., no detection. (F) Blood glucose excursions and the AUC scores in fasting Bsg+/+ and Bsg–/– female mice during lactate tolerance tests (n = 7–11/genotype). (G) Blood glucose excursions and AUC scores during pyruvate tolerance tests in female mice (n = 8–10/genotype). (H) Endogenous glucose production in isolated hepatocytes of Bsg+/+ and Bsg–/– female mice cultured in medium supplemented with 20 mM sodium lactate and 2 mM sodium pyruvate in the absence or presence of 100 nM AZD3965 (an inhibitor of MCT1 activity). n = 6 for independent experiments. For all relevant panels, data are presented as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, for the comparison of Bsg+/+ and Bsg–/– at the indicated time point (2-tailed unpaired Student’s t test).