Fig 1.

A: There was a 70% reduction in LKB1 expression in LKB1-KO hearts (†: P<0.01 vs. control, N=8–18). The lox-sites did not affect LKB1 expression and Lox and Lox/+ mice were used as controls. B: Phosphorylation of AMPK-Thr¹⁷² was inhibited in LKB1-KO hearts under both basal and ischemic conditions (a: P<0.01 vs. basal.*: P<0.05 vs. control, N=5–8) C: This was associated with ablated AMPKα2-activity (a: P<0.01 vs. basal.†: P<0.01 vs. control, N=5–8) while D: Ischemia increased AMPKα1-activity among all genotypes (a: P<0.01 vs. basal, N=5–8). E and F: Knock out of LKB1 increased expression of AMPKα2 and α1 (*: P<0.05 and †: P<0.01 vs. control, N=8–18).