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<blockquote data-quote="phoenix" data-source="post: 619277" data-attributes="member: 12578"><p>There appear to be progenitor cells in the pancreas which may be able to become new working islet cells.</p><p>Until recently it was thought that in non diabetics cells in the pancreas were like neurons and simply died off with age and were not replaced . It was thought that cells were replaced very slowly by division and those that were killed off by gluco/lipotoxicity or autoimmune attack were could not be replaced since completely new cells were not formed after childhood/adolescence.</p><p>However in mouse models they have been able to show that new cells were 'grown' in a damaged pancreas. <a href="http://www.betacell.org/content/articleview/article_id/114/" target="_blank">http://www.betacell.org/content/articleview/article_id/114/</a></p><p> </p><p>There are other studies that seem to support this view (not completely unchallenged though).</p><p>It is also known that initially the beta cell mass increases in those that become obese (that's why all overweight people don't become diabetic) Indeed beta cell mass increases during normal pregnancy. This means that there must be either new cells formed or increased cell division and some sort of signals in the body that causes this to take place.</p><p> They have also discovered that very long term Type 1s have some insulin producing islets (very small amounts that couldn't be detected by earlier techniques)</p><p>However, the autoimmune 'attack' may continue as has been demonstrated in islet cell replacement therapies, one theory is that cells may be produced and then killed off continuously. What is clear is that the process is very slow and doesn't provide very large numbers of new cells.</p><p>(that's why an important field of research is how to encapsulate and protect implanted cells to stop them from just being killed off again)</p><p> </p><p>How to reprogram progenitor cell to increase functional beta cell mass is very much a target of international research.</p><p>These are the aims of the 'beta cell consortium'</p><ol> <li data-xf-list-type="ol">Use cues from pancreatic development to directly differentiate pancreatic beta cells and islets from stem/progenitor cells for use in cell-replacement therapies for diabetes,</li> <li data-xf-list-type="ol">Determine how to stimulate beta cell regeneration in the adult pancreas as a basis for improving beta cell mass in diabetic patients,</li> <li data-xf-list-type="ol">Determine how to reprogram progenitor/adult cells into pancreatic beta-cells both in-vitro and in-vivo as a mean for developing cell-replacement therapies for diabetes, and</li> <li data-xf-list-type="ol">Investigate the progression of human type-1 diabetes using patient-derived cells and tissues transplanted in humanized mouse models.</li> </ol><p><a href="http://www.betacell.org/research/" target="_blank">http://www.betacell.org/research/</a></p></blockquote><p></p>
[QUOTE="phoenix, post: 619277, member: 12578"] There appear to be progenitor cells in the pancreas which may be able to become new working islet cells. Until recently it was thought that in non diabetics cells in the pancreas were like neurons and simply died off with age and were not replaced . It was thought that cells were replaced very slowly by division and those that were killed off by gluco/lipotoxicity or autoimmune attack were could not be replaced since completely new cells were not formed after childhood/adolescence. However in mouse models they have been able to show that new cells were 'grown' in a damaged pancreas. [url]http://www.betacell.org/content/articleview/article_id/114/[/url] There are other studies that seem to support this view (not completely unchallenged though). It is also known that initially the beta cell mass increases in those that become obese (that's why all overweight people don't become diabetic) Indeed beta cell mass increases during normal pregnancy. This means that there must be either new cells formed or increased cell division and some sort of signals in the body that causes this to take place. They have also discovered that very long term Type 1s have some insulin producing islets (very small amounts that couldn't be detected by earlier techniques) However, the autoimmune 'attack' may continue as has been demonstrated in islet cell replacement therapies, one theory is that cells may be produced and then killed off continuously. What is clear is that the process is very slow and doesn't provide very large numbers of new cells. (that's why an important field of research is how to encapsulate and protect implanted cells to stop them from just being killed off again) How to reprogram progenitor cell to increase functional beta cell mass is very much a target of international research. These are the aims of the 'beta cell consortium' [LIST=1] [*]Use cues from pancreatic development to directly differentiate pancreatic beta cells and islets from stem/progenitor cells for use in cell-replacement therapies for diabetes, [*]Determine how to stimulate beta cell regeneration in the adult pancreas as a basis for improving beta cell mass in diabetic patients, [*]Determine how to reprogram progenitor/adult cells into pancreatic beta-cells both in-vitro and in-vivo as a mean for developing cell-replacement therapies for diabetes, and [*]Investigate the progression of human type-1 diabetes using patient-derived cells and tissues transplanted in humanized mouse models. [/LIST] [url]http://www.betacell.org/research/[/url] [/QUOTE]
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