I can see I am sending some folks nuts into the deep end of the used nuclear fuel rod swimming pool.
What keeps getting missed in their argument is this:
For type ones who have deficit of insulin and I believe rarely have glucose saturation of the skeletal muscles and as a result little insulin resistance in effect, adding insulin usually/always works.
For type 2's suffering glucose saturation most of time, adding insulin can be a frustrating no action result leaving excess insulin rotating around a type 2 body till some of the saturation of the skeletal muscle cells drops down and insulin receptors of muscle cells go back to accepting insulin.
Using met to slow down liver glucose release works irregardless of insulin resistance and stops excess liver glucose at source.
Diet and hearty exercise as well help get glucose burned off skeletal muscles temp storage sites ( reduce insulin resistance) so they (skeletal muscle temp glucose storage) can go back to storing more glucose and regulating blood glucose. Controlling blood glucose is always a storage function that insulin drives.
In a distributed muscle/glucose storage site - some muscles will have room for more glucose, others will not. Those muscles with no room turn on insulin resistance - downgrade cell insulin receptor sites to prevent a muscle cell glucose storage site getting overloaded with glucose and poisoning the cell.
Type 1 and type 2 are not same disease even if they share some similarities in possible treatment options.
This also explains why actos can always force more glucose into muscle cells when added insulin appears dead or useless.