Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.7554/eLife.13828 http://scihub22266oqcxt.onion/10.7554/eLife.13828 C4871705!4871705!27092792     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       eLife 2016 ; 5 (ä): ä Nephropedia Template TP {{tp|p=27092792|t=2016. Blockade of glucagon signaling prevents or reverses diabetes onset only if residual ?-cells persist |pdf=|usr=}}{{27092792}} gab.com Text Blockade of glucagon signaling prevents or reverses diabetes onset only if residual -cells persist JO: eLife http://www.kidney.de/pget.php?&tw=1&pmid=27092792 #FOAvip Glucagon secretion dysregulation in diabetes fosters hyperglycemia. Recent studies report that mice lacking glucagon receptor (Gcgr-/-) do not develop diabetes following streptozotocin (STZ)-mediated ablation of insulin-producing ?-cells. Here, we show that diabetes prevention in STZ-treated Gcgr-/- animals requires remnant insulin action originating from spared residual ?-cells: these mice indeed became hyperglycemic after insulin receptor blockade. Accordingly, Gcgr-/- mice developed hyperglycemia after induction of a more complete, diphtheria toxin (DT)-induced ?-cell loss, a situation of near-absolute insulin deficiency similar to type 1 diabetes. In addition, glucagon deficiency did not impair the natural capacity of ?-cells to reprogram into insulin production after extreme ?-cell loss. ?-to-?-cell conversion was improved in Gcgr-/- mice as a consequence of ?-cell hyperplasia. Collectively, these results indicate that glucagon antagonism could i) be a useful adjuvant therapy in diabetes only when residual insulin action persists, and ii) help devising future ?-cell regeneration therapies relying upon ?-cell reprogramming.DOI:http://dx.doi.org/10.7554/eLife.13828.001 Twit Text FOAVip Blockade of glucagon signaling prevents or reverses diabetes onset only if residual -cells persist ????eLife http://www.kidney.de/pget.php?&tw=1&pmid=27092792 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27092792 #FOAvip English Wikipedia <ref>{{Cite pmid|27092792}}</ref> Blockade of glucagon signaling prevents or reverses diabetes onset only if residual ?-cells persist #MMPMID27092792 Damond N; Thorel F; Moyers JS; Charron MJ; Vuguin PM; Powers AC; Herrera PL eLife 2016[]; 5 (ä): ä PMID27092792show ga Glucagon secretion dysregulation in diabetes fosters hyperglycemia. Recent studies report that mice lacking glucagon receptor (Gcgr-/-) do not develop diabetes following streptozotocin (STZ)-mediated ablation of insulin-producing ?-cells. Here, we show that diabetes prevention in STZ-treated Gcgr-/- animals requires remnant insulin action originating from spared residual ?-cells: these mice indeed became hyperglycemic after insulin receptor blockade. Accordingly, Gcgr-/- mice developed hyperglycemia after induction of a more complete, diphtheria toxin (DT)-induced ?-cell loss, a situation of near-absolute insulin deficiency similar to type 1 diabetes. In addition, glucagon deficiency did not impair the natural capacity of ?-cells to reprogram into insulin production after extreme ?-cell loss. ?-to-?-cell conversion was improved in Gcgr-/- mice as a consequence of ?-cell hyperplasia. Collectively, these results indicate that glucagon antagonism could i) be a useful adjuvant therapy in diabetes only when residual insulin action persists, and ii) help devising future ?-cell regeneration therapies relying upon ?-cell reprogramming.DOI:http://dx.doi.org/10.7554/eLife.13828.001 äBlockade of glucagon signaling prevents or reverses diabetes onset onl(epmc).pdf DeepDyve Pubget Overpricing