I dismiss the role of lactic acidosis since, as I understand it, lactic acidosis occurs as an effect rather than cause of DKA.
This leaves two possibilities: (1) relative increased ratio of production to utilization of ketones in DKA (either absolute ratio or ratio of rate); or (2) the pH change is wholly attributable to the dehydration caused by glucosuria in DKA.
I could make a story for either of these, but it's also possible there's some other contributing factor like kidney damage that I'm missing.
Anyone have any insights? Please reply.