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10.7554/eLife.13828 http://scihub22266oqcxt.onion/10.7554/eLife.13828 C4871705!4871705 !27092792     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27092792 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Elife 2016 ; 5 (?): ? 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. 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[Apr]; 5 (?): ? PMID27092792 show 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. |*Signal Transduction [MESH] |Animals [MESH] |Diabetes Mellitus, Experimental/physiopathology [MESH] |Gastrointestinal Agents/*metabolism [MESH] |Glucagon/*metabolism [MESH] |Insulin-Secreting Cells/*drug effects/metabolism [MESH] |Insulin/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH]Blockade of glucagon signaling prevents or reverses diabetes onset onl(epmc).pdf DeepDyve Pubget Overpricing