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I haven’t read anything on this subject that says precisely this. I’m just piecing together things I have read from various sources. So, this is more in the nature of a question than a statement of what I know. Lets hope this is not a well recognized theory already.

It would seem to me that these two diabetics came to their situation along two different roads. The classical obese diabetic (Type II) began producing excess levels of insulin while still young. My understanding is that this is triggered by high levels of emotion in childhood. These high levels of insulin production drove insulin resistance as the cells down-regulated to block the infusion of too much glucose. So, with IR, even moderate levels of circulating glucose was forced into the fat cells where the glucose would be stored as fat. So, excessively high insulin levels drive insulin resistance, drive fattening. And after 40 years of living and driving the beta cells excessively, their output finally can not keep pace with the ever increasing levels of insulin resistance. There is a clinical diagnosis of diabetes. After some period of time as a diabetic the Beta cells begin to exhaust themselves and the diabetic reality becomes increasingly unreversible.

The lean diabetic suggests there was no long period of insulin over-production. I say this because that would have fattened the individual. So, it would seem that the lean diabetic is not a consequence of years of over-producing insulin, but rather some event at some time in the individuals life that reduced the strength of the beta cells. It's likely, as I see it, that these individuals may display no insulin resistance at all. The end result of becoming insulin dependent may be the same. But, how these two individuals arrived there are completely different. I welcome any comments.
 

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I haven’t read anything on this subject that says precisely this. I’m just piecing together things I have read from various sources. So, this is more in the nature of a question than a statement of what I know. Lets hope this is not a well recognized theory already.

It would seem to me that these two diabetics came to their situation along two different roads. The classical obese diabetic (Type II) began producing excess levels of insulin while still young. My understanding is that this is triggered by high levels of emotion in childhood. These high levels of insulin production drove insulin resistance as the cells down-regulated to block the infusion of too much glucose. So, with IR, even moderate levels of circulating glucose was forced into the fat cells where the glucose would be stored as fat. So, excessively high insulin levels drive insulin resistance, drive fattening. And after 40 years of living and driving the beta cells excessively, their output finally can not keep pace with the ever increasing levels of insulin resistance. There is a clinical diagnosis of diabetes. After some period of time as a diabetic the Beta cells begin to exhaust themselves and the diabetic reality becomes increasingly unreversible.

The lean diabetic suggests there was no long period of insulin over-production. I say this because that would have fattened the individual. So, it would seem that the lean diabetic is not a consequence of years of over-producing insulin, but rather some event at some time in the individuals life that reduced the strength of the beta cells. It's likely, as I see it, that these individuals may display no insulin resistance at all. The end result of becoming insulin dependent may be the same. But, how these two individuals arrived there are completely different. I welcome any comments.
It's a case of RELATIVE insulin resistance. IR is not one thing. The one we usually talk about is "peripheral" (mostly muscle). But, the liver can also be insulin resistant. That doesn't mean it fails to uptake glucose like muscle. Rather, it means that it doesn't respond to insulin telling it to stop secreting glucose. It continues to do so when it shouldn't, causing blood sugar to rise. Finally, there's the fat cells. Insulin tells them to take in fatty acids and re-assemble them into triglycerides for storage. Insulin resistance in this third case means fat cells are less able to add to their storage.

So, if adipose (fat cell) insulin resistance is relatively higher than the other two, the result is a skinny T2 diabetic. If, on the other hand it is lower - meaning fat cells are MORE responsive to insulin than the other two, the T2 will be fat. That's all there is to it.
 
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Discussion Starter #3
I hadn't realized there could be resistance to the passage into the fat cells. Presumably this blocks both fatty acids and glucose. Most diabetics are familiar with the toxicity that builds up when glucose rises in the blood. But I don't recall any mention of what would occur if fatty acids rose too high. Is this when people have high levels of Triglyceride?
 

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I hadn't realized there could be resistance to the passage into the fat cells. Presumably this blocks both fatty acids and glucose. Most diabetics are familiar with the toxicity that builds up when glucose rises in the blood. But I don't recall any mention of what would occur if fatty acids rose too high. Is this when people have high levels of Triglyceride?
High-carb eaters, including diabetics, will likely have high triglycerides as well and low HDL, but the bigger issue here relating to toxicity is free fatty acids, not TriG. You might not find everything I said in one place, but you can Google all three kinds of insulin resistance and find lots of stuff you can piece together. I don't know if fat cells uptake glucose for their own energy, maybe they do, but that's irrelevant to adipose insulin resistance. The main function of insulin vis-a-vis fat cells is pushing fat in for storage. When they're insulin resistant, this is impaired. If one has more of the other two, there will be lots of extra glucose around. In that situation, the liver will convert more of it to fat via de novo lipogenesis and the insulin (now higher attempting to compensate for the other two IRs) pushes more of this fat into storage causing weight gain. When they become too resistant and/or too "full" they can't hold on to their stores, free fatty acids rise in circulation and eventually end up in muscle cells, liver and pancreas, further increasing the other two kinds of IR.
 
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This is interesting. I read somewhere that an increase of insulin resistance in fat cells tended to lower it in muscle cells. I need to read more, may be next weekend before I have time.
 
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