While you’re technically right, I don’t see the point. Insulin secretion is minimal in the fasting state, so why would you need to dabble with insulin resistance?
Many Diabetes drugs, like PPAR agonists, stimulate Insulin sensitivity, but where do they do it? The body has PPAR receptors pretty much everywhere EXCEPT in the Muscles, so patients taking these drugs & continuing to consume excessive amounts of Carbohydrates are basically switching on every mechanism they can to make sure all of their calories are being stored as Fat.
These drugs were approved by the FDA based on surrogate endpoints (they reduce Insulin resistance!) but they increase the risk of having a Heart attack by something like 28%, so I think we really need to question whether decreasing Insulin resistance without any finer specification (ie, in Muscle vs. Fat, Fasting vs. Post-prandial) is the goal we want to have in mind. Maybe it is just solving 1 part of a bigger problem & exacerbating other parts of that problem.
While you’re technically right, I don’t see the point. Insulin secretion is minimal in the fasting state, so why would you need to dabble with insulin resistance?
Many Diabetes drugs, like PPAR agonists, stimulate Insulin sensitivity, but where do they do it? The body has PPAR receptors pretty much everywhere EXCEPT in the Muscles, so patients taking these drugs & continuing to consume excessive amounts of Carbohydrates are basically switching on every mechanism they can to make sure all of their calories are being stored as Fat.
These drugs were approved by the FDA based on surrogate endpoints (they reduce Insulin resistance!) but they increase the risk of having a Heart attack by something like 28%, so I think we really need to question whether decreasing Insulin resistance without any finer specification (ie, in Muscle vs. Fat, Fasting vs. Post-prandial) is the goal we want to have in mind. Maybe it is just solving 1 part of a bigger problem & exacerbating other parts of that problem.