AKT1 and diabetes mellitus: 1) Regulate L-arginine/NO pathway, act as an NO donor to cause relaxation 2) regulate the NO/cGMP pathway, restore the corpus cavernosum endothelial function 3) inhibit oxidative stress, restore Akt activity, protect endothelial and smooth muscle cells (diabetes-induced ED) 4) enhance NO release from corpus cavernosum endothelial and nerve cell 5) increase serum testosterone levels 6) activate large conductance Ca2+-activate K+ (BKCa) channels in corporal smooth muscle cells 7) decrease HIF-1α expression in hypoxia state 8) increase eNOS expression 9) inhibit PDE5A