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Beta Cell De-Differentiation?
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<blockquote data-quote="Oldvatr" data-source="post: 2488659" data-attributes="member: 196898"><p>My research so far has allowed me to accept the term de-differentiation as being the corruption, removal or replacement of the mRNA code in the Beta cell which stops the cell from performing its original programmed function. I have found no evidence that the function changes to the Alpha Cell function. The experimental evidence from the ND study shows that simple dietary intervention can reverse the deprogramming and restore normal beta cell operation, so the corruption or change that occurred is not permanent. Most interventions such as toxins, radiation, virus etc that damage cells is permanent and the cell must be renewed / replaced through the normal autophhage process. Beta cells do not have this mechanism.</p><p></p><p>In vivo observations of T2D progression shows that beta cells do not get replaced under normal operations of the body. The body does not repair damaged ,RNA code, which requires gene splicing in vitro outside the body. Therefore the theory that de-differentiation in T2D leads to Beta cells changing to perform Alpha Cell operation is incorrect. The claim that the ND diet causes recovery back to beta cell operation by reversing that theorised process is also incorrect.</p><p></p><p>One thing I discovered in my research which i did not know is that recent studies have shown that beta cells not only respond to the GLUT enzymes for operation, but also have a GLP-1 receptor that also triggers an insulin excretion cycle. Other research has also demonstrated that Alpha cells secrete not just glucagon, but also GLP-1 under certain circumstances. GLP-1 has a half life of 2 minutes, so there is srong coupling between the alpha and beta cells in this respect. The conditions for this to happen appear to be very high glucose levels even when the alpha cell is still producing glucagon. This appears to be an emergency stop correction factor since normally GLP-1 is produced by the gut in the presence of protein and fat metabolism and normally is triggering insulin for adipose storage to occur in the absence of a carb intake (i.e. carnivore and the fed state)</p><p><a href="https://www.sciencedirect.com/science/article/pii/S2212877820300880" target="_blank">https://www.sciencedirect.com/science/article/pii/S2212877820300880</a></p><p><a href="http://www.glucagon.com/GLP-1%20and%20the%20Alpha%20Cell.html" target="_blank">http://www.glucagon.com/GLP-1 and the Alpha Cell.html</a></p><p></p><p>I think this mechanism may explain the sleep post meal syndrome that has been reported elsewhere in the Forum, and may be a mechanism involved in RH diadetes.</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 2488659, member: 196898"] My research so far has allowed me to accept the term de-differentiation as being the corruption, removal or replacement of the mRNA code in the Beta cell which stops the cell from performing its original programmed function. I have found no evidence that the function changes to the Alpha Cell function. The experimental evidence from the ND study shows that simple dietary intervention can reverse the deprogramming and restore normal beta cell operation, so the corruption or change that occurred is not permanent. Most interventions such as toxins, radiation, virus etc that damage cells is permanent and the cell must be renewed / replaced through the normal autophhage process. Beta cells do not have this mechanism. In vivo observations of T2D progression shows that beta cells do not get replaced under normal operations of the body. The body does not repair damaged ,RNA code, which requires gene splicing in vitro outside the body. Therefore the theory that de-differentiation in T2D leads to Beta cells changing to perform Alpha Cell operation is incorrect. The claim that the ND diet causes recovery back to beta cell operation by reversing that theorised process is also incorrect. One thing I discovered in my research which i did not know is that recent studies have shown that beta cells not only respond to the GLUT enzymes for operation, but also have a GLP-1 receptor that also triggers an insulin excretion cycle. Other research has also demonstrated that Alpha cells secrete not just glucagon, but also GLP-1 under certain circumstances. GLP-1 has a half life of 2 minutes, so there is srong coupling between the alpha and beta cells in this respect. The conditions for this to happen appear to be very high glucose levels even when the alpha cell is still producing glucagon. This appears to be an emergency stop correction factor since normally GLP-1 is produced by the gut in the presence of protein and fat metabolism and normally is triggering insulin for adipose storage to occur in the absence of a carb intake (i.e. carnivore and the fed state) [URL]https://www.sciencedirect.com/science/article/pii/S2212877820300880[/URL] [URL]http://www.glucagon.com/GLP-1%20and%20the%20Alpha%20Cell.html[/URL] I think this mechanism may explain the sleep post meal syndrome that has been reported elsewhere in the Forum, and may be a mechanism involved in RH diadetes. [/QUOTE]
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