The first two questions are a little more difficult to answer. But, I will detail the first one for you.
The mechanism of insulin resistance is as such:
There are insulin receptors on a cell membrane, once insulin binds to an insulin receptor, endocytosis occurs where the insulin/insulin receptor complex is absorbed by the cell and the insulin hormone is degraded by lysosomes. Around 90% of the insulin receptors are recycled from this process and sent back to the cell membrane to continue the cycle.
The problem arises when insulin receptors are continuously saturated with the presence of insulin.
Lets use an arbitrary number of 100 for the number of insulin receptors on a given cell. If all 100 of those receptors are saturated and undergo endocytosis and 90% of those receptors are recycled that will leave 90 receptors on the cell membrane. If those 90 receptors are saturated and undergo endocytosis and 90% of those receptors are recycled that will leave 81 receptors. So on and so forth.
The reduction of insulin receptors is effectively what leads to insulin resistance. The body needs time to replenish insulin receptors and the way to do this is by an absence of insulin for a given amount of time.
There are autoimmune situations where antibodies attach to insulin receptors, rending them incapable of performing their function. This isn't very common to my understanding. But, this would also result in a form of insulin resistance, essentially.