AKT1 and type 2 diabetes mellitus: Later, we surprisingly found in brains harvested from these same HFF, ob/ob, and Het‐MλKO mice and also in brains of obese/T2DM monkeys, that, contrary to the speculation that the brain is insulin‐resistant and hypoinsulinized in states of systemic insulin resistance, the activity of the brain IR and activities of both Akt and PKC‐λ/ι are all maximally activated, by basal resting hyperinsulinemia.15, 68