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Title : A new paradigm of insulin resistance - DT2 13
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A new paradigm of insulin resistance - DT2 13

our current paradigm of insulin resistance is a key. Insulin is a hormone that acts on a hormone receptor on a cell surface in order to have an effect.

This is often referred to as pattern lock and key. The blockade is the insulin receptor that keeps the doors to the closed cell. When the proper key (insulin) is inserted, then the door is opened to allow blood glucose within the cell. This glucose is then able to feed the machinery of the cell.

Once you remove the key (insulin), then the door closed again and glucose in the blood is no longer able to go inside the cell.

What happens during the phenomenon of insulin resistance? Classically, we imagine that the key no longer fit well. The key (insulin) is able to open the lock (receptor) but only partially and not very well. As a result, glucose is not able to pass through the door normally.

This results in lower than normal amounts of glucose into the cell. Glucose, which is now blocked by the closed door, piles up outside the cell in the blood, which can detect blood sugar so high and make the clinical diagnosis of type 2 diabetes

This it has also been described as a state of internal starvation because the cell has little glucose inside. The automatic reaction is to the body to increase insulin production (key). Since each key works as well as before, the body produces an excess amount of keys to ensure that enough glucose to enter cells. A good orderly theory.

The problem, really, is that this paradigm does not really fit the reality. First, there is the problem of insulin or the insulin receptor? Well, it's really very easy these days to examine the structure of the insulin receptor and the structure of insulin patients insulin resistance. Just isolate insulin or some cells and check their molecular structure with fancy tools. It becomes immediately clear that there is nothing wrong, either with insulin or receiver. So what's the deal?

The only remaining possibility is that something is gumming up the system. Some programs block that interferes with the mechanism of the lock and key. But what? There are all kinds of theories. Inflammation. Oxidative stress. For advanced glycation end products. All usual fashion words that arise when doctors really have no idea. With this model, we have no fucking real feel what caused the insulin resistance. Without understanding what causes IR, we have no chance to treat it.

Then there is the central paradox of hepatic insulin resistance. Let me explain. Insulin has two main actions in the liver. Remember that insulin goes up when eating. It tells the body to stop production in the liver glucose (gluconeogenesis) because there is a lot of glucose coming in the stomach (food). This is mediated through the pathway Fox01.

The second important action in the liver is increased sebum production (de novo Lipogeneis (DNL)). This is to cope with the flood of entry of glucose that the body can not use properly. This is mediated through the route of SREBP-1c.

Therefore, if the liver becomes resistant to insulin, then the effect of insulin should fall for these two actions. That is, the liver must follow to make glucose, and stop making fat. But that's only the case of gluconeogenesis. That is, during insulin resistance, the liver continues to make new glucose as expected. But DNL (making new fat) continues and actually increases. Thus the effect of insulin on the DNL blunts but not accelerated!

What the hell?

How can this hell seven liver insulin resistant be selectively resistant to insulin effect even accelerate the effect of the other? In the same cell, in response to the same levels of insulin, the insulin receptor same? That seems crazy. The same cell is insulin resistance and super-sensitive insulin at the same time!

How can we explain this paradox?

need a new paradigm of insulin resistance that best fits the facts. In fact, we can think of insulin resistance as a phenomenon overflow , instead of a lock and a key. All we really know about insulin resistance is that it is much harder to move glucose into a "insulin resistant" than a normal cell.

But this does not necessarily mean that the door is stuck . instead, perhaps the cell is already filled with glucose and therefore more glucose can not enter.

Imagine the cell to be a subway car. When the door opens, passengers the outer part (glucose) in the blood march nice orderly manner in the wagon empty meter (cell). Normally, actually not much requires a push to this glucose into the cell (insulin gives thrust).

However, during insulin resistance, the problem is not that the door will not open. the problem, however, is that the subway car (cell) is already filled with passengers (glucose) . Now, glucose outside the cell simply can not enter and leave crowded on the platform.

Insulin tries to push glucose into the cell as the Japanese subway pushers, but simply can not do it because it is full. Therefore, it appears that the cell is resistant to the effects of insulin, but in reality the problem is that the cell is already overflowing. Thus, the knee jerk reaction is to produce more insulin (buttons) to help push glucose into the cell. What works, but only for a while.

Therefore, the cell is not in a state of "internal starvation". Instead, the cell is filled with glucose. Glucose starts spilling out blood which resembles the gluconeogenesis has not stopped which is consistent with insulin resistance However, insulin and its receptor are fine;. are simply overwhelmed by the exogenous glucose 'toxicity'

But what happens. with fat production?

in the classical model of insulin resistance, the paradox is that DNL is enhanced, not diminished that much like insulin sensitivity rather than added strength. but in the model overflow, the DNL would be higher because the cell is trying to get rid of excess glucose by producing extra fat. the cell is overflowing and not in a mode of "inner hunger."

Why is this critical? Due to the understanding of this new paradigm will lead to the answer of how insulin resistance and what you can do about that develops. The problem lies not with insulin or the insulin receptor. Both are standard. The problem is that the cell is completely stuffed full of glucose. So, what caused it? The answer then seems obvious - is a matter of excess glucose and excess insulin. In other words, insulin itself was caused insulin resistance. We do not need to chase shadows for some mysterious cause of insulin resistance.

Once we understand that excess glucose and excessive insulin is the cause of insulin resistance, then we can now devise a rational treatment. Reduce insulin and reduce glucose. Once insulin resistance, cure diabetes type 2.

is reversed


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