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. 2022 Aug 24;9:957549. doi: 10.3389/fmolb.2022.957549

FIGURE 1.

FIGURE 1

AMPK DKI mouse model and phenotypic effects of disrupting whole-body AMPK-glycogen interactions on maximal running speed and body composition. (A) Schematic of WT mice with intact AMPK-glycogen binding and AMPK DKI mice in which critical tryptophan residues within the AMPK β subunit isoforms that mediate glycogen binding (β1; predominantly expressed in mouse liver; and β2 predominantly expressed in mouse skeletal muscle) have been mutated to alanine (β1 W100A and β2 W98A, respectively), resulting in whole-body disruption of AMPK-glycogen binding; (B) Maximal running speed (m/min); (C) Total body mass (g); (D) Total lean mass (g); (E) Total fat mass (g). *: p < 0.05, **: p < 0.01, ****p < 0.0001; values are represented as mean ± SEM; n = 21–23 mice per group.