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10.1038/nature13633 http://scihub22266oqcxt.onion/10.1038/nature13633 C4209186!4209186!25141178     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2014 ; 514 (7523): 503-7 Nephropedia Template TP {{tp|p=25141178|t=2014. Diabetes Recovery By Age-Dependent Conversion of Pancreatic ?-Cells Into Insulin Producers |pdf=|usr=}}{{25141178}} gab.com Text Diabetes Recovery By Age-Dependent Conversion of Pancreatic -Cells Into Insulin Producers JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=25141178 #FOAvip Total or near-total loss of insulin-producing ?-cells is a situation found in diabetes (Type 1, T1D) 1,2. Restoration of insulin production in T1D is thus a major medical challenge. We previously observed in mice in which ?-cells are completely ablated that the pancreas reconstitutes new insulin-producing cells in absence of autoimmunity 3. The process involves the contribution of islet non-?-cells; specifically, glucagon-producing ?-cells begin producing insulin by a process of reprogramming (transdifferentiation) without proliferation 3. Here we studied the influence of age on ?-cell reconstitution from heterologous islet cells after near-total ?-cell loss. We found that senescence does not alter ?-cell plasticity: ?-cells can reprogram to produce insulin from puberty through adulthood, and also in aged individuals, even a long-time after ?-cell loss. In contrast, prior to puberty there is no detectable ?-cell conversion, although ?-cell reconstitution after injury is more efficient, always leading to diabetes recovery; it occurs through a newly discovered mechanism: the spontaneous en masse reprogramming of somatostatin-producing ?-cells. The younglings display ?somatostatin-to-insulin? ?-cell conversion, involving de-differentiation, proliferation and re-expression of islet developmental regulators. This juvenile adaptability relies, at least in part, upon combined action of FoxO1 and downstream effectors. Restoration of insulin producing-cells from non-?-cell origins is thus enabled throughout life via ?- or ?-cell spontaneous reprogramming. A landscape with multiple intra-islet cell interconversion events is emerging, thus offering new perspectives. Twit Text FOAVip Diabetes Recovery By Age-Dependent Conversion of Pancreatic -Cells Into Insulin Producers ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=25141178 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25141178 #FOAvip English Wikipedia <ref>{{Cite pmid|25141178}}</ref> Diabetes Recovery By Age-Dependent Conversion of Pancreatic ?-Cells Into Insulin Producers #MMPMID25141178 Chera S; Baronnier D; Ghila L; Cigliola V; Jensen JN; Gu G; Furuyama K; Thorel F; Gribble FM; Reimann F; Herrera PL Nature 2014[Oct]; 514 (7523): 503-7 PMID25141178show ga Total or near-total loss of insulin-producing ?-cells is a situation found in diabetes (Type 1, T1D) 1,2. Restoration of insulin production in T1D is thus a major medical challenge. We previously observed in mice in which ?-cells are completely ablated that the pancreas reconstitutes new insulin-producing cells in absence of autoimmunity 3. The process involves the contribution of islet non-?-cells; specifically, glucagon-producing ?-cells begin producing insulin by a process of reprogramming (transdifferentiation) without proliferation 3. Here we studied the influence of age on ?-cell reconstitution from heterologous islet cells after near-total ?-cell loss. We found that senescence does not alter ?-cell plasticity: ?-cells can reprogram to produce insulin from puberty through adulthood, and also in aged individuals, even a long-time after ?-cell loss. In contrast, prior to puberty there is no detectable ?-cell conversion, although ?-cell reconstitution after injury is more efficient, always leading to diabetes recovery; it occurs through a newly discovered mechanism: the spontaneous en masse reprogramming of somatostatin-producing ?-cells. The younglings display ?somatostatin-to-insulin? ?-cell conversion, involving de-differentiation, proliferation and re-expression of islet developmental regulators. This juvenile adaptability relies, at least in part, upon combined action of FoxO1 and downstream effectors. Restoration of insulin producing-cells from non-?-cell origins is thus enabled throughout life via ?- or ?-cell spontaneous reprogramming. A landscape with multiple intra-islet cell interconversion events is emerging, thus offering new perspectives. äDiabetes Recovery By Age-Dependent Conversion of Pancreatic ?-Cells In(epmc).pdf DeepDyve Pubget Overpricing