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Physiology of insulin release - know your pancreas
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<blockquote data-quote="Oldvatr" data-source="post: 2486355" data-attributes="member: 196898"><p>About 10 mmol/l is what the IGTT test uses to ensure first phase response. When an arginine block is in place then the level is over 20 mmol/l before the pancreas releases insulin,</p><p></p><p>Thank you for posting. There is a typo in ~Table 1</p><p>Section V is of interest which is describing the voltage controlled switching that controls insulin generation and release.</p><p></p><p>Although it mentions granules, it does not make it clear that these store insulin locally in the pancreas and it is this store that is released during the First Phase insulin response. The granules hold insulin in hexameric form i.e. 6 insulins attached to a glycerol stem in the pancreas granules,</p><p></p><p>I think but am not certain, that the reason why the ND weight loss program improved the P#1` insulin response was that the granules or the messaging path got blocked off by the fatty tissue, which cleared due to the intervention. so IMO the apparent loss of P#1 response may be a storage problem in the beta cell, and this does not need the mind bending theory of beta cell de-differentiation to explain it. The solution may be quite simple.</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 2486355, member: 196898"] About 10 mmol/l is what the IGTT test uses to ensure first phase response. When an arginine block is in place then the level is over 20 mmol/l before the pancreas releases insulin, Thank you for posting. There is a typo in ~Table 1 Section V is of interest which is describing the voltage controlled switching that controls insulin generation and release. Although it mentions granules, it does not make it clear that these store insulin locally in the pancreas and it is this store that is released during the First Phase insulin response. The granules hold insulin in hexameric form i.e. 6 insulins attached to a glycerol stem in the pancreas granules, I think but am not certain, that the reason why the ND weight loss program improved the P#1` insulin response was that the granules or the messaging path got blocked off by the fatty tissue, which cleared due to the intervention. so IMO the apparent loss of P#1 response may be a storage problem in the beta cell, and this does not need the mind bending theory of beta cell de-differentiation to explain it. The solution may be quite simple. [/QUOTE]
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