I ran into someone the other day asking me about how first phase insulin response affects type 2 diabetes, and since this isn't something we've talked about much on the site yet, I thought it would be a good topic unto itself.
In normal people, our beta cells store insulin during fasting in preparation for a meal. The meal itself initially elevates blood glucose levels. The beta cells sense this and release this stored insulin into our blood, which helps combat the first wave of blood glucose that is appearing during a meal.
I think that there are some people that think that when we eat a meal, all the glucose from it is released at once, but the process of digestion does take time, and as the meal is digested and processed, glucose is released accordingly. Once digestion is complete, and the duration of this depends on one's digestion by the way, then we revert back to internal mechanisms of glucose regulation, the liver for instance, to continue to provide us with the glucose we need.
We don't have to constantly eat though to survive because of this internal blood sugar regulation, and when this is working properly it will release glucose slowly into the bloodstream as needed, and we always need to maintain our blood sugar lest it go low and we suffer, and even die if it's low enough.
In those without blood sugar issues, without blood sugar dysregulation, stored glucose and glucose made from non glucose sources gets released, which is regulated by both the hormones insulin and glucagon, and both are kept in balance to provide us with the fuel, the blood sugar that we need, regardless of whether we're eating or haven't eaten for a long time.
The primary role of insulin isn't to lower our blood sugar actually, it's to store energy, and this is why too much insulin in the presence of too much to store ends up packing on the pounds. So when we eat a meal, most of this will end up being stored, as the body's needs don't depend on the meal, they depend on other factors such as our level of activity and our metabolic rate.
This doesn't change when we eat, other than of course the fact that we tend to be sitting down and are therefore less active during meals, but the need for glucose isn't determined by its supply. So if we have sufficient insulin secretion, we store the excess, as glycogen and as fat.
Due to the way that we tend to eat, not grazing but consuming larger portions of food in a single sitting, we will be taking in more than we need at the time, so the main mechanism of insulin here is to store what is not needed. This is important because it's not to just get rid of the glucose from our blood, as some people think, it's to do something with it.
So we want the meal to be stored, and that part actually really only depends on secreting enough insulin to do the job. People who don't make enough insulin, type 1 diabetics and late stage type 2 diabetics who have become like type 1's, double diabetics in other words, lose their capacity for this storage.
So when this happens one will lose weight, and one's weight is therefore quite reliable in looking at whether we make too much or too little insulin, particularly if you don't make enough. In this case you will lose weight, period. If you make too much you will generally gain weight but not always.
The reason why you don't always gain weight with high insulin is that one's metabolism matters here, if for instance you are hyperthyroid the extra insulin will promote storage but one's metabolic demands are higher so your needs are higher. If you are hypothyroid though, you will have a tendency to gain more weight than normal, but in this case insulin is still involved, you have to store it in the first place and insulin is involved in that but so is our requirements, but being overweight is still a reliable marker for insulin levels regardless, and in fact low thyroid in itself affects insulin levels, by increasing insulin resistance.
So what about first phase insulin secretion? Well people tend to worry a lot more about this than they should, as in the grand scheme of things, our initial secretion isn't particularly significant. Sure, without proper phase 1 your glucose levels will rise a bit more initially, but that's about it. Once insulin levels get high enough, then you have enough, and at this point it's no longer lack of insulin, although it is during the delay.
A good analogy here is that let's say that there is a truck making a delivery at a warehouse and the driver is piling boxes at the door. So if there's no one there to move them or less workers initially they will pile up. If the proper amount of workers finally come along they will keep up although it may take them a bit longer to put all the goods away.
So the magnitude here isn't very significant, as first phase insulin only represents a small amount of the overall insulin secreted in response to the meal, so a few boxes get put there before we start moving them away in other words. What happens with type 2 typically is that the work may start slow but there are quite a few more workers on the scene a little later, and this is because there is more to do, extra merchandise from the liver is being added, stuff that doesn't belong, and even with the extra workers they often still can't keep up with the extra work.
In the next article I want to go into more why we have a diminished or absent phase 1 insulin response, but I first need to point out that this is only a minor issue when we look at the entire problem, and insulin itself, the lack of insulin at this time, wouldn't even be that noteworthy if not for this excess load that our livers provide. However we still need to look at what role insulin is playing here which we'll continue with next time.