Ok, so i just posted this on another comment thread, but I wanted to put it here and ask for any assistance or correction because this is how I understand insulin resistance to begin to happen (or one way at least), but please correct me if I'm wrong.
If we have too much glucose being used for ATP in the cell to use at that time, a byproduct begins to build up called citrate. Citrate begins to signal phosphofructokinase to stop taking in all that glucose, and it begins to send it elsewhere, ie another muscle or your liver. Now, when your liver (70g) and muscle (200g) glycogen stores are full, your body needs to do something with the continued carbohydrates. The muscle cell then converts the excess carbs to glyceraldehyde 3 phosphate, and when three of those hook up, you get a triglyceride. Your body then stores this as fat in adipose tissue. Since your body can only do this so fast, glucose begins to stack up in your blood stream, so your body produces more insulin. But since your body doesn't WANT any more glucose in the muscle cells (because it's trying to actually have LESS that it currently has), it begins to decrease the number of insulin receptors on the muscle cell, but the insulin receptors on your adipose cells stay intact. This is the beginning of insulin resistance, and why we will feel hungry all the time, because our cells begin to starve, whereas our fat cells continue to grow and take in all the glucose that our cells would need. As far as I believe, anyway. Am I off here?
asked byCoachCanadan (2393)
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