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. Author manuscript; available in PMC: 2015 Feb 4.
Published in final edited form as: Cell Metab. 2014 Feb 4;19(2):272–284. doi: 10.1016/j.cmet.2013.12.001

Figure 1. Hepatic glucose metabolism in the absence of BAD.

Figure 1

(A) Glucose-stimulated lactate production by primary Bad +/+ and −/− hepatocytes (n=5–8).

(B) Glucose release by Bad +/+ and −/− hepatocytes treated with lactate/pyruvate (n=6).

(C) PTT in Bad +/+ and −/− mice (n=14–20).

(D) Lactate production in Bad knockdown hepatocytes 8 hr after glucose stimulation (n=9).

(E) Glucose production in Bad knockdown hepatocytes treated with lactate/pyruvate (n=3–5).

(F) PTT in C57BL/6J mice after hepatic knockdown of Bad (n=12–17).

(G–H) Relative hepatic mRNA levels of Pck1 (G) and L-Pk (H) in fed and overnight fasted C57BL/6J mice after hepatic knockdown of Bad (n=10).

(I) PTT in C57BL/6J mice after hepatic knockdown of Gk (n=8–12).

(J–K) Relative hepatic mRNA levels of Pck1 (J) and L-Pk (K) in fed and overnight fasted C57BL/6J mice after hepatic knockdown of Gk (n=5).

Error bars, ± SEM. *p < 0.05; **p < 0.01, ***p < 0.001.

See also Figure S1.