Type 2 diabetics tend to have much higher levels of glucagon, which is the other hormone secreted by the pancreas, and is the one that is implicated as the major culprit in diabetes, at least at the level of what is directly producing high blood sugar levels.
A lot of people think, well when we have high blood sugar than this is because our insulin isn't effective enough, you read that all the time, but the real reason here is that our livers are secreting way too much glucose, more than we can handle even with high levels of insulin.
So high levels of glucagon is primarily responsible for this, and when we measure glucagon levels in type 2 diabetics, we see clearly that they are too high. Oddly enough, even with all we know about the way glucagon works, how elevated levels produce high blood sugar, and even though none of this is in any doubt, we don't talk about glucagon levels much or bother even thinking about them much.
So the best that conventional medicine can do here is to give you something like metformin which does limit excess liver dumping to some degree, it cuts it down by a third on average, but you're still left with the two thirds, and this is why metformin, in spite of helping a fair bit, isn't a miracle drug by any means.
If it eliminated excess liver dumping, well that would actually even be a cure for diabetes, as it's been shown that without excess liver dumping, we could eat even a high carb diet and our blood sugars would be fine. That's how big a deal excess glucagon is.
So when we eat a meal, our blood sugars can go way up there, and most people think, well it's because we can't handle the carbs from the meal, but as it turns out, this is when glucagon secretion is at its highest, and we take the sugar from the meal and dump a whole bunch of extra in there and that's something we can't handle.
Of course this doesn't mean that reducing carbs isn't effective in limiting after meal blood sugar spikes, it really does help actually, but that's because we aren't piling on too much glucose from the meal on top of the liver dumping we get.
So this brings us to why our pancreases are secreting too much glucagon. Well our alpha cells, the ones that secrete this stuff, are supposed to be sensitive to insulin enough to have insulin levels regulate this.
If we are insulin resistant though, guess what happens? The alpha cells are insulin resistant as well, and these cells are not the ones you want to be insulin resistant, as they have the power to increase your blood sugar in a way that can elevate your blood sugar dramatically.
Type 1 diabetics equip themselves with injectable glucagon, and in an emergency, when nothing else will save them, injecting glucagon can, because nothing raises blood sugar like glucagon, not even all the glucose tablets you can choke down, and if it were that simple than all they would need to do is chew the tablets. Glucagon works a lot better though, it will command the liver to secrete huge amounts of glucose into the blood immediately, in a way that can save your life, it's that effective.
So what happens to cause this insulin resistance in our alpha cells? Well like insulin resistance elsewhere, there are a number of things that go wrong, but the biggest one is elevated free fatty acids, or FFAs. This is something I haven't spoken about yet but I'll be saying much more about this as it plays a huge role in diabetes.
So the alpha cells are particularly sensitive to excess FFAs, lipotoxicity in other words, or having them poisoned by too much fat. You can check out a very good scientific article on this here, although this is not something that's any secret, FFAs cause insulin resistance period, and that's well known, and the fact that it does it in our alpha cells is no surprise at all.
FFAs by the way are very interesting, since they not only cause insulin resistance, they also increase insulin secretion, and so therefore, at least temporarily, the insulin resistance it causes is compensated for by higher insulin, which can keep blood sugar normal. The reason why a lot of obese people can have insulin resistance but not have high blood sugar is thought to be from this mechanism.
Higher insulin though in itself causes insulin resistance, so it's not hard to see how this all can break down over time. Even more interesting though is the role that high insulin plays with FFA levels, it increases them. Normal insulin levels don't, but when you see your insulin levels go up, and they tend to go way up with us, well this is bad news for fatty acid metabolism.
So while it's interesting to note the effect of FFA on insulin resistance in general, we have been focused a lot on this causing insulin resistance in the liver, and we haven't really looked that much at it causing insulin resistance in the alpha cells, which is even more significant as far as effects on blood sugar goes.
The big thing if we're going to solve this though is to start by looking to reduce excessive insulin levels, as this is a big factor in increasing serum FFA, as is a high carb diet, which both increases insulin and provides fuel for this fire.
It's worth noting that AMPK, which is an enzyme that is very important in blood sugar control, and something that diabetics are low in, has been shown to really affect the alpha cells in particular, and this explains in part the benefits of increasing this, although this is just one of the things that AMPK does, but given that AMPK plays a big role in fat metabolism, this is not surprising.
You may just want to say that excess fat accumulation is to blame here, things like obesity and fatty organs, but what we need to keep in mind is what causes this stuff, and the main cause is, guess what, high insulin levels and a high carb diet.
So once again, it's not that we have not enough insulin, it's that we have too much, and alpha cell insulin resistance, lipotoxity, and the increased glucagon secretion that results is yet another effect of this, but a huge one.