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Beta Cell De-Differentiation?
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<blockquote data-quote="Oldvatr" data-source="post: 2487755" data-attributes="member: 196898"><p>The takeaway from that last report is of interest (edited to remove external references)</p><p>"</p><p><span style="font-size: 15px"><strong> Effects of adipocytes on β-cell differentiation and function</strong></span></p><p>The direct crosstalk between pancreatic adipocytes and islets has not yet been studied in depth </p><p>Using the insulin secreting cell line Min6 and 3T3-L1 adipocytes in a co-culture system, a downregulation of glucokinase<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/glucokinase" target="_blank"> </a>of the KATP-channel protein Kir6.2, and of insulin has been observed <em>. In vitro</em> exposure of human islets to preadipocytes and adipocytes in a co-culture system revealed that mRNA levels of islet differentiation markers (islet specific hormones, PDX-1 and GLUT-2) did not change <a href="https://www.sciencedirect.com/science/article/pii/S2212877819301760#bib1" target="_blank">[1]</a>. The theory that fat cells do not affect β-cell differentiation is further corroborated by the unaltered <em>in situ</em> immunostaining for insulin,glucagon and somatostatin of islets in the neighborhood of fat cells. Of note, this method may not be sensitive enough to detect changes of hormone storage until the reduction is already well advanced. Hormone content, moreover, may not correlate with the ability to secrete insulin in response to glucose. "</p><p>In simple terms, they did not find any evidence that fat cell secretome altered cell differentiation in alpha, beta or delta pancreatic cells. No change. No deprogramming At the same time they noted downregulation of function in the samples ie reduced c-peptide and reduced insulin output. This is not to be read as proof, because they probably only examined a small portion of the sample. Only that it was not seen. important that they confirmed this finding from the mRNA itself</p></blockquote><p></p>
[QUOTE="Oldvatr, post: 2487755, member: 196898"] The takeaway from that last report is of interest (edited to remove external references) " [SIZE=4][B] Effects of adipocytes on β-cell differentiation and function[/B][/SIZE] The direct crosstalk between pancreatic adipocytes and islets has not yet been studied in depth Using the insulin secreting cell line Min6 and 3T3-L1 adipocytes in a co-culture system, a downregulation of glucokinase[URL='https://www.sciencedirect.com/topics/medicine-and-dentistry/glucokinase'] [/URL]of the KATP-channel protein Kir6.2, and of insulin has been observed [I]. In vitro[/I] exposure of human islets to preadipocytes and adipocytes in a co-culture system revealed that mRNA levels of islet differentiation markers (islet specific hormones, PDX-1 and GLUT-2) did not change [URL='https://www.sciencedirect.com/science/article/pii/S2212877819301760#bib1'][1][/URL]. The theory that fat cells do not affect β-cell differentiation is further corroborated by the unaltered [I]in situ[/I] immunostaining for insulin,glucagon and somatostatin of islets in the neighborhood of fat cells. Of note, this method may not be sensitive enough to detect changes of hormone storage until the reduction is already well advanced. Hormone content, moreover, may not correlate with the ability to secrete insulin in response to glucose. " In simple terms, they did not find any evidence that fat cell secretome altered cell differentiation in alpha, beta or delta pancreatic cells. No change. No deprogramming At the same time they noted downregulation of function in the samples ie reduced c-peptide and reduced insulin output. This is not to be read as proof, because they probably only examined a small portion of the sample. Only that it was not seen. important that they confirmed this finding from the mRNA itself [/QUOTE]
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