Insulin is chiefly removed by receptor-mediated endocytosis and proteolysis (the receptor organizes a vesicle being pinched off from the cell membrane with the insulin inside, and then the contents of the vesicle can be digested).

Insulin acts by binding to the insulin receptor on the outside of cells, so it isn't otherwise "used up" when it acts. Since a homeostatic signal isn't much good if you can't turn it down/off again, that breakdown mechanism is important.

Being pedantic, but I wouldn't frame it this way. The pathologies in those conditions aren't that insulin levels are too high (barring accidental/intentional overdose), but a deficient effect.

There are feedback mechanisms that titrate secretion to response in cases of insulin resistance, therefore prolonged hyperglycaemia promotes insulin secretion.

Type 1 is typically due to a deficiency of insulin for various reasons.

[removed]

Insulin has a lifetime of about 5-6 minutes in the bloodstream - it is degraded by the insulin-sensitive tissues and also by the liver.

If somebody has insulin resistance or type 2 diabetes, they have hyperinsulinemia. This is because their body is constantly producing excess insulin because their liver is producing excess glucose.