Can u cure type 1 diabetes symptoms,medicine of diabetes in patanjali yogpeeth,helen free home diabetes test 4.9,eating too much sugar causes type 2 diabetes - Review

Our current paradigm of insulin resistance is that of a lock and key, and it's simply wrong. Insulin is a hormone that acts upon a hormonal receptor on a cell surface in order to have an effect. Once you remove the key (insulin) then the gate closes back up and glucose in the blood is no longer able to go inside the cell. This has also been described as a state of internal starvation since the cell has little glucose on the inside.
The second major action in the liver is to increase the production of fat (De Novo Lipogenesis (DNL)). So, if the liver becomes insulin resistant, then the effect of insulin should drop for both of these actions.
How in seven hells can this insulin resistant liver selectively be resistant to one effect of insulin yet accelerate the effect of the other? Insulin tries to push the glucose into the cell like the Japanese Subway Pushers, but they simply can't do it because it's full. In the classic model of insulin resistance, the paradox was that DNL was enhanced, not decreased which looked a lot like heightened insulin sensitivity instead of resistance. Once we understand that excessive glucose and excessive insulin is the cause of the insulin resistance, then we can now devise a rational treatment. I am working on a document outlining strategies for monitoring and surveillance of antimicrobial resistance (hence the recent plethora of posts on the topic! As we pause to celebrate Christmas and New Year, we wish to thank all of you for coming to TheMarioBlog each day. When the proper key (insulin) is inserted, then the gate opens to let glucose from the blood inside the cell. The glucose, which is now blocked by the closed gate, piles up outside the cell in the blood, which we can detect as elevated blood sugar and make the clinical diagnosis of type 2 diabetes. In the very same cell, in response to the very same levels of insulin, with the very same insulin receptor?
In fact, we can think of insulin resistance as an overflow phenomenon, instead of a lock and key one.
Instead, perhaps the cell is already overflowing with glucose and therefore more glucose cannot go in. When the door opens, the passengers on the outside (glucose in the blood) march in a nice orderly manner into the empty subway car (cell).

The problem, instead is that the subway car (cell) is already overflowing with passengers (glucose).
So, it looks like the cell is resistant to the effects of the insulin, but really the problem is that the cell is already overflowing.
But in the overflow model, the DNL would be enhanced because the cell is trying to rid itself of the excess glucose by producing extra fat.
Because understanding this new paradigm will lead to the answer of how insulin resistance develops and what we can do about it.
The key (insulin) is able to open the lock (receptor) but only partially and not very well.
Since each key works less well than previously, the body over-produces the number of keys to make sure that enough glucose goes into the cells. Well, it's really quite easy these days to look at the structure of insulin and the structure of the insulin receptor of insulin resistance patients.
All we really know about insulin resistance is that it is much more difficult to move glucose into an 'insulin resistant' cell than a normal one.
Normally, it doesn't really require much of a push to get this glucose into the cell (insulin gives the push).
So, the knee jerk reaction is to manufacture more insulin (pushers) to help push glucose into the cell.
Glucose starts spilling into the blood, which looks like gluconeogenesis has not been stopped consistent with insulin resistance. I have the dreaded cold and so feel mildly unwell and filled with sneezes, so I am wrapped up in a blanket and feeling sorry for myself. You simply isolate the insulin or some cells and check their structure with fancy molecular tools.
It immediately becomes clear that there is nothing wrong with either the insulin or the receptor. It tells the body to stop producing glucose in the liver (gluconeogenesis) because there is lots of glucose coming in from the stomach (food).

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