I have been trying to understand what appears to be at the heart of Type 2 diabetes and that is insulin resistance. Put simply this is an inefficiency in the mechanisms controlled by insulin that remove glucose from the blood.
You aren't necessarily diabetic if you have insulin resistance (IR) but IR forces the pancreas to produce more insulin and it becomes a vicious circle until not enough excessive insulin is produced to efficiently to remove glucose from the blood effectively and it's the resulting high residual glucose that is personified in Type 2 diabetes.
But what exactly is insulin resistance? This was a mystery to me for quite some time but if I am right the answer is that it is several things. There is tissue IR, which is the reluctance by fat cells and muscle cells to respond to insulin and absorb and store glucose from the blood. But it seems that by far the most powerful factor is liver insensitivity to insulin. When the liver becomes insensitive to insulin it adds too much glucose when there is demand and doesn't shut off the supply as quickly as it should when the demand subsides.
So how do you improve insulin sensitivity? It seems that for muscle and fat tissue exercise to maintain or increase muscle mass and losing weight, perhaps to add sugar storage capacity to fat cells, are the obvious strategies? I'm not sure that's exactly correct and where that's the case I'd love someone to clarify this. For liver insensitivity to insulin it appears that exercise and muscle building are again important because of a link to human growth hormone (which acts on Insulin-like Growth Factor (IGF)). I don't fully understand the mechanism but IGF receptors in the liver trigger the liver's glucose production but the receptors don't work properly when the liver is insulin resistant.
So I'm now speculating completely - but this problem with the IGF receptors in the livers of insulin resistant people seems to be linked to fatty livers (which have become fatty because of eating more carbs than the body cab deal with and some people have lower carb thresholds than others.
I do, therefore, wonder if the benefit of getting rid of fat in and around the liver to reverse diabetes factors (like the Newcastle diet) to a degree involves the de-fatting of these IGF receptors?
If anyone would like to jump in here - you're most welcome!
You aren't necessarily diabetic if you have insulin resistance (IR) but IR forces the pancreas to produce more insulin and it becomes a vicious circle until not enough excessive insulin is produced to efficiently to remove glucose from the blood effectively and it's the resulting high residual glucose that is personified in Type 2 diabetes.
But what exactly is insulin resistance? This was a mystery to me for quite some time but if I am right the answer is that it is several things. There is tissue IR, which is the reluctance by fat cells and muscle cells to respond to insulin and absorb and store glucose from the blood. But it seems that by far the most powerful factor is liver insensitivity to insulin. When the liver becomes insensitive to insulin it adds too much glucose when there is demand and doesn't shut off the supply as quickly as it should when the demand subsides.
So how do you improve insulin sensitivity? It seems that for muscle and fat tissue exercise to maintain or increase muscle mass and losing weight, perhaps to add sugar storage capacity to fat cells, are the obvious strategies? I'm not sure that's exactly correct and where that's the case I'd love someone to clarify this. For liver insensitivity to insulin it appears that exercise and muscle building are again important because of a link to human growth hormone (which acts on Insulin-like Growth Factor (IGF)). I don't fully understand the mechanism but IGF receptors in the liver trigger the liver's glucose production but the receptors don't work properly when the liver is insulin resistant.
So I'm now speculating completely - but this problem with the IGF receptors in the livers of insulin resistant people seems to be linked to fatty livers (which have become fatty because of eating more carbs than the body cab deal with and some people have lower carb thresholds than others.
I do, therefore, wonder if the benefit of getting rid of fat in and around the liver to reverse diabetes factors (like the Newcastle diet) to a degree involves the de-fatting of these IGF receptors?
If anyone would like to jump in here - you're most welcome!