When you have Type 2 diabetes and you have been told that you have it because your pancreas either fails to make enough insulin or that the insulin that it makes is not able to be used properly (that’s a mouthful), have you ever thought to yourself, “Huh?”
Has this information been filed away in the part of your brain labeled, “Information I don’t understand and sounds too confusing to learn,” just waiting to be purged when possible? Whenever I hear a patient being told this I often wonder if they’re going to ask, “Well, which is it, do I make too much insulin or not enough, and why does this happen?” I think if I had diabetes I would want to know. Let me see if I can explain it here.
I will start off by reminding you that it takes approximately 10 years to go from completely normal to actually having diabetes. I am sure this varies somewhat from person to person, however on average it takes 10 years.
After you eat a meal that has sugar in it, the sugar will enter the blood stream. In response to sugar entering the blood the beta cells, located throughout the pancreas, start making insulin. Typically, the greater the amount of sugar that enters the blood, the greater the amount of insulin produced by the beta cells in the pancreas. At least, this is the way it is supposed to work.
The insulin produced in the beta cells then enters the blood stream and looks for some sugar. Once it finds a sugar molecule it swims over and grabs a hold of it. (A little-known fact is that insulin only has one arm, so it can only grab ahold of one sugar.) The insulin then takes the sugar out of the blood vessel and over to a muscle, fat or liver cell. Once close to the cell the insulin starts heading over to one of the cell’s many doors. The insulin then opens the door to the cell and escorts the sugar inside. Once this is accomplished the insulin is not reused and is basically put out to pasture. Meanwhile, other insulins are finding sugar in the blood and taking them to other muscle, fat and liver cells, thereby returning the level of sugar in the blood to pre-meal levels. Once blood sugar levels are back to normal the beta cells stop making insulin (except for little drips of insulin that constantly leak from the liver into the blood throughout the day) until sugar enters the blood stream again, perhaps after the next meal.
In the case of Type 2 diabetes, about 10 years before actually developing the disease, when insulin tries to open the doors so that the sugar can enter, the insulin finds that the doors have become much more difficult to open, and one insulin is no longer enough to get the doors open (I call this rusty hinges. Officially it is called the onset of insulin resistance.) This means the beta cells must make additional insulin to help get the doors open due to their rusty hinges. Over the course of the next 10 years, or thereabouts, increasing amounts of insulin are required to get the doors to the cells open so that the sugar can enter. (This is why you hear that you may be making plenty of insulin, however, it is not being used properly.)
Eventually, these beta cells that have been working so hard begin to fail (as would anything that is working in a manner in which it is not designed) and insulin production drops as a result. (This is when you hear that you are not making enough insulin.) As a result of this reduction in insulin production, sugar can no longer enter the cells as it is supposed to and remains trapped in the blood stream.
So you see, in the development of Type 2 diabetes, there is an overproduction of insulin followed by a reduction in insulin production.
Original Post from: http://www.huffingtonpost.com/milt-bedingfield/type-2-diabetes_b_1684246.html?utm_source=twitterfeed&utm_medium=twitter