The underlying mechanisms explaining the associations between BST and glycemic control are still relatively unknown, but acute light exercise bouts may activate alternative molecular signals that can bypass defects in insulin signaling in skeletal muscle, resulting in an insulin-independent increase in glucose uptake (Stanford and Goodyear, 2014) through several signal transduction pathways (Sylow et al., 2016), including the AMPK signaling network (Kjobsted et al., 2017), a function that remains intact in T2D patients (Kjobsted et al., 2016). This evidence concerns the gene INS and type 2 diabetes mellitus.