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10.1111/dom.12341 http://scihub22266oqcxt.onion/10.1111/dom.12341 C4159727!4159727!25200302     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Diabetes+Obes+Metab 2014 ; 16 (0 1): 96-101 Nephropedia Template TP {{tp|p=25200302|t=2014. The search for the mechanism of early sympathetic islet neuropathy (eSIN) in autoimmune diabetes |pdf=|usr=}}{{25200302}} gab.com Text The search for the mechanism of early sympathetic islet neuropathy (eSIN) in autoimmune diabetes JO: Diabetes Obes Metab http://www.kidney.de/pget.php?&tw=1&pmid=25200302 #FOAvip This review outlines our search for the mechanism causing the early loss of islet sympathetic nerves in autoimmune diabetes. Since our previous work has documented the importance of autonomic stimulation of glucagon secretion during hypoglycaemia, the loss of these nerves may contribute to the known impairment of this specific glucagon response early in human type 1 diabetes. We therefore briefly review the contribution that autonomic activation, and sympathetic neural activation in particular, makes to the subsequent glucagon response to hypoglycaemia. We also detail evidence that animal models of autoimmune diabetes mimic both the early loss of islet sympathetic nerves and the impaired glucagon response seen in human type 1 diabetes. Using data from these animal models, we examine mechanisms by which this loss of islet nerves could occur. We provide evidence that it is not due to diabetic hyperglycaemia, but it is related to the lymphocytic infiltration of the islet. Ablating the p75 neurotrophin receptor, which is present on sympathetic axons, prevents eSIN, but, interestingly, not diabetes. Thus, we appear to have separated the immune-related loss of islet sympathetic nerves from the immune-mediated destruction of islet ?-cells. Finally, we speculate on a way to restore the sympathetic innervation of the islet. Twit Text FOAVip The search for the mechanism of early sympathetic islet neuropathy (eSIN) in autoimmune diabetes ????Diabetes Obes Metab http://www.kidney.de/pget.php?&tw=1&pmid=25200302 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25200302 #FOAvip English Wikipedia <ref>{{Cite pmid|25200302}}</ref> The search for the mechanism of early sympathetic islet neuropathy (eSIN) in autoimmune diabetes #MMPMID25200302 Taborsky GJ; Mei Q; Hackney DJ; Mundinger TO Diabetes Obes Metab 2014[Sep]; 16 (0 1): 96-101 PMID25200302show ga This review outlines our search for the mechanism causing the early loss of islet sympathetic nerves in autoimmune diabetes. Since our previous work has documented the importance of autonomic stimulation of glucagon secretion during hypoglycaemia, the loss of these nerves may contribute to the known impairment of this specific glucagon response early in human type 1 diabetes. We therefore briefly review the contribution that autonomic activation, and sympathetic neural activation in particular, makes to the subsequent glucagon response to hypoglycaemia. We also detail evidence that animal models of autoimmune diabetes mimic both the early loss of islet sympathetic nerves and the impaired glucagon response seen in human type 1 diabetes. Using data from these animal models, we examine mechanisms by which this loss of islet nerves could occur. We provide evidence that it is not due to diabetic hyperglycaemia, but it is related to the lymphocytic infiltration of the islet. Ablating the p75 neurotrophin receptor, which is present on sympathetic axons, prevents eSIN, but, interestingly, not diabetes. Thus, we appear to have separated the immune-related loss of islet sympathetic nerves from the immune-mediated destruction of islet ?-cells. Finally, we speculate on a way to restore the sympathetic innervation of the islet. äThe search for the mechanism of early sympathetic islet neuropathy (eS(epmc).pdf DeepDyve Pubget Overpricing