Cell composition and gene-expression dynamics of skeletal muscle regeneration after contraction-induced injury

Small-molecule activators targeting the allosteric drug and metabolite (ADaM) site of AMPK enhance insulin-independent glucose uptake in skeletal muscle and promote blood glucose lowering in preclinical models of hyperglycemia. The regulatory AMPKγ subunit plays a central role in energy sensing, and the skeletal muscle-selective γ3 isoform is essential for AMP/ZMP-induced glucose uptake, but not for ADaM site activators. We hypothesized that the predominant γ1 isoform is required for ADaM site activator-stimulated glucose uptake in skeletal muscle.