Recently, I learned that one of the causes of Type II diabetes is that insulin receptors on cell surfaces lose their sensitivity due to long-term high exposure to insulin (which occurs as a result of high blood sugar).
How do receptors (like that for insulin) become more resistant to ligands? Is the receptor itself getting damaged? If so, how, and why don't other frequently activated proteins/receptors (like GPCR's) also get damaged? If not, then how does the cell become more "resistant" to insulin?