Off the top of my head, I know that syndrome X is theorized to be caused by insulin resistance. A quick Google shows that hyperinsulinemia (note the spelling) can also be caused by insulin resistance. Insulin tolerance sounds too much like a synonym for insulin resistance for me to bother looking up. PCOS is also associated with insulin resistance.
Just in case you’re confused, the syndrome we’re talking about here is having an endocrine system that overreacts to insulin.
There are a number of states which cause insulin sensitivity.
If a person has a deficiency of cortisol or thyoxine, they will be, effectively, insulin sensitive. Indeed, such individuals tend to have mild hypoglycemia.
People with complete, or near-complete, absence of (anterior) pituitary function can be quite insulin sensitive and even develop overt hypoglycemia.
IIRC, congenital absence of glucagon leads to such severe insulin sensitivity that fatal hypoglycemia is the rule.
People with diabetes due to pancreatic destruction or absence (eg. pancreatitis or pancreatectomy) often have exquisitely precarious glucose control. They need insulin and are diabetic due to the absence of insulin. Yet, in the absence of glucagon and hence in the presence of associated insulin sensitivity, even an extra half unit of insulin can cause profound hypoglycemia.
Exercise, or more accurately, ‘the recent post exercise state’ is a day-to-day, physiologic state of increased insulin sensitivity. Diabetics on insulin often develop hypoglycemia due to exercise (this is prevented by taking in more calories peri-exercise or taking less insulin). Of more widepsread importance is the fact that virtually anyone who exercises becomes more insulin sensitive. Hence, it’s a great way to offset some of the insulin resistance of type II diabetes or the so-called metabolic syndrome. Likewise, it’s a great way to lessen the burden on the insulin secreting beta cells of the pancreas. By increasing insulin sensitivity via exercise, less insulin is needed. This may help sustain beta cell function and thus prevent the development of frank diabetes (NB: the difference between plain insulin resistance and type II diabetes is that in the latter, the beta cells can no longer keep up with the extra demand to secrete insulin which has been necessitated by the insulin resistant state. Conversely, even with astronomical degrees of insulin resistance, the sugar barely rises, if at all, so long as the beta cell remains healthy enough to produce enough insulin to meet the insulin resistance).
On rereading my post (above) an hour later, I realize that I should have explicitly noted that the increased insulin sensitivity which is present following pancreatic destruction (pancreatitis) or absence of the pancreas (pancreatectomy) is due to loss of glucagon. In other words, glucagon, like insulin, is made in the pancreas.