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Beta Cell De-Differentiation?
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<blockquote data-quote="Oldvatr" data-source="post: 2488145" data-attributes="member: 196898"><p>Indeed, The remission objective declared for all his studies was meeting fasting levels of below 48 mmol/l. </p><p></p><p>The Springer paper you linked is one I have studied, and it is actually an IGTT, i.e. intravenous not oral. It has some errors in it that I have raised with Prof Taylor, and he has declared that the error although systemic, is not significant. I discussed this in another thread last year,</p><p></p><p>The one I have not discussed with him is that others doing the same type of test have shown that their results are nowhere near as spectacular because the IGTT process has less effect when compared to the tradiitional OGTT, Some have found that the IGTT may be missing some of the enzyme triggers associated woth the First Stage insulin response that is triggered by amylase secreted in the saliva, which of course is missing in the intravenous technique. There may be other enzymes and incretins that the gut secretes that are also going to be missing.</p><p></p><p>The beta cell output technique he adopted uses an arginine bolus to block the output channel thus damming up the normal secretion in the local granules. When the clamp is removed, then there is a sudden flood from the stored insulin, Unfortunately, the output capacity test followed a normal GTT cycle, and the timing is such that the second test was overlapping the residue from the first test. The two tests were not uncoupled sufficiently and is not representative of normal activity. Therefore his conclusions regarding first and second phase respnses are not reliable IMO. </p><p></p><p>What he has in my opinion achieved is to show that the capacity in tems of storing and releasing a full 'bladder' is probably demonstrated, and the improvement from the weight loss can be claimed, but the mechanism cannot. I.e. the removal of ectopic fat in the pancreas will be of benefit in clearing signalling pathways, emptying cells and capilliaries blocked or chocked by the fat. The actual beta cell capacity may not be changing at all, just the delivery system. in other words he is measuring the contents of the storage warehouse, not the ability of the production line to produce in response to a step demand change.</p><p></p><p>Lastly, which I noted the other day, he has a typo that is most unfortunate in a final report. He refers to the insulin responses in terms of T1D not T2D A minor mishap.</p><p></p><p>I think overall there is much to commend this work, its just the conclusions and explanations following it that i have a quibble with.</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 2488145, member: 196898"] Indeed, The remission objective declared for all his studies was meeting fasting levels of below 48 mmol/l. The Springer paper you linked is one I have studied, and it is actually an IGTT, i.e. intravenous not oral. It has some errors in it that I have raised with Prof Taylor, and he has declared that the error although systemic, is not significant. I discussed this in another thread last year, The one I have not discussed with him is that others doing the same type of test have shown that their results are nowhere near as spectacular because the IGTT process has less effect when compared to the tradiitional OGTT, Some have found that the IGTT may be missing some of the enzyme triggers associated woth the First Stage insulin response that is triggered by amylase secreted in the saliva, which of course is missing in the intravenous technique. There may be other enzymes and incretins that the gut secretes that are also going to be missing. The beta cell output technique he adopted uses an arginine bolus to block the output channel thus damming up the normal secretion in the local granules. When the clamp is removed, then there is a sudden flood from the stored insulin, Unfortunately, the output capacity test followed a normal GTT cycle, and the timing is such that the second test was overlapping the residue from the first test. The two tests were not uncoupled sufficiently and is not representative of normal activity. Therefore his conclusions regarding first and second phase respnses are not reliable IMO. What he has in my opinion achieved is to show that the capacity in tems of storing and releasing a full 'bladder' is probably demonstrated, and the improvement from the weight loss can be claimed, but the mechanism cannot. I.e. the removal of ectopic fat in the pancreas will be of benefit in clearing signalling pathways, emptying cells and capilliaries blocked or chocked by the fat. The actual beta cell capacity may not be changing at all, just the delivery system. in other words he is measuring the contents of the storage warehouse, not the ability of the production line to produce in response to a step demand change. Lastly, which I noted the other day, he has a typo that is most unfortunate in a final report. He refers to the insulin responses in terms of T1D not T2D A minor mishap. I think overall there is much to commend this work, its just the conclusions and explanations following it that i have a quibble with. [/QUOTE]
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