>>...stored in the liver as the molecule known as glycogen

I'd point out that a major storage location for glycogen is skeletal muscle - but the muscle needs to be able to absorb glucose.

Gerald Shulman has done NMR work showing that insulin resistance in skeletal muscles comes from a variation of diglycerol (a triglyceride with one FA removed) interfering with the chain reaction that starts with the presence of insulin at the cell membrane and ends with GLUT4 transporters poked through the membrane. More insulin is required to overcome this blockage - which might shed some light on why the 'extra' insulin is produced.

Exercise (and chromium picolinate?) can activate an alternate pathway that activates GLUT4 , but I'd expect that if a muscle cell is pulling in glucose for immediate respiration it isn't storing it as glycogen.

Shulman points out that in humans IR starts in skeletal muscles and eventually spreads to the liver - but the order is reversed in mice. He also posits (in an interview with Peter Attia) that exercise long term can reverse IR in skeletal muscles.

BTW, Shulman references Jerry Reaven’s 1988 Banting Lecture, which I’m sure you’re familiar with, but for anyone else, I found a link to a PDF of it.

Also (off topic) I’ve recently learned that the blood brain barrier system includes GLUT1 receptors to pass glucose to the CS fluid. These don’t need insulin, but can be downregulated (which seems to mean fewer of them, not less active — but I could have that wrong) in the presence of high blood glucose, protecting the CNS. Meanwhile the astrocytes (support cells that convert glucose into lactate, pass that on to neurons as a fast-respiratory ‘fuel’) have GLUT4 (insulin dependent) receptors. I’m not a researcher, but I wonder what happens if the BBB GLUT1s are downregulated (high glucose) and the astrocyte GLUT4s (spreading IR) are blocked…?