Short version that makes insulin sensitivity improvement mechanism of GLP clearer.
When insulin receptors on muscle cells and elsewhere are exposed to insulin for extended periods of time, they downregulate by withdrawing behind the cell wall. It’s TIME of exposure to insulin, not intensity of exposure that makes them become less sensitive. As insulin sensitivity goes down, insulin has to stay elevated for longer and longer for glucose to clear, which makes receptors down regulate even more. A vicious cycle. It’s why insulin sensitivity typically worsens with age. Eventually beta cells can burn out, now you can’t even produce enough insulin, and the “insulin tap” stays open longer and longer, trying to get cells to respond, sensitivity keeps worsening, and here comes diabetes.
GLPs makes beta cells release a lot more insulin than they normally would in response to blood sugar rising.
Cells get this “loud” insulin signal and quickly soak up excess glucose from blood, then insulin release quickly shuts off. So instead of a slow trickle of insulin, requiring a long time for glucose to be cleared, it’s a quick, intense pulse. This happens so fast insulin receptors don’t have time to withdraw. In fact, over time the insulin receptors interpret this as “not receiving enough insulin signal”, and respond by sticking out further, becoming more sensitive. The longer this “intense short burst” type of insulin release goes on (by staying on a GLP), the better insulin sensitivity becomes.