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10.3892/ijmm.2015.2207 http://scihub22266oqcxt.onion/10.3892/ijmm.2015.2207 C4494597!4494597!25976560     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       Int+J+Mol+Med 2015 ; 36 (1): 173-85 Nephropedia Template TP {{tp|p=25976560|t=2015. Endogenous GLP-1 as a key self-defense molecule against lipotoxicity in pancreatic islets |pdf=|usr=}}{{25976560}} gab.com Text Endogenous GLP-1 as a key self-defense molecule against lipotoxicity in pancreatic islets JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25976560 #FOAvip The number of pro-? cells is known to increase in response to ? cell injury and these cells then generate glucagon-like peptide-1 (GLP-1), thus attenuating the development of diabetes. The aim of the present study was to further examine the role and the mechanisms responsible for intra-islet GLP-1 production as a self-protective response against lipotoxicity. The levels of the key enzyme, prohormone convertase 1/3 (PC1/3), as well as the synthesis and release of GLP-1 in models of lipotoxicity were measured. Furthermore, islet viability, apoptosis, oxidative stress and inflammation, as well as islet structure were assessed after altering GLP-1 receptor signaling. Both prolonged exposure to palmitate and a high-fat diet facilitated PC1/3 expression, as well as the synthesis and release of GLP-1 induced by ? cell injury and the generation of pro-? cells. Prolonged exposure to palmitate increased reactive oxygen species (ROS) production, and the antioxidant, N-acetylcysteine (NAC), partially prevented the detrimental effects induced by palmitate on ? cells, resulting in decreased GLP-1 levels. Furthermore, the inhibition of GLP-1 receptor (GLP-1R) signaling by treatment with exendin-(9-39) further decreased cell viability, increased cell apoptosis and caused a stronger inhibition of the ? cell-specific transcription factor, pancreatic duodenal homeobox 1 (PDX1). Moreover, treatment with the GLP-1R agonist, liraglutide, normalized islet structure and function, resulting in a decrease in cell death and in the amelioration of ? cell marker expression. Importantly, liraglutide maintained the oxidative balance and decreased inflammatory factor and p65 expression. Overall, our data demonstrate that an increase in the number of pro-? cells and the activation of the intra-islet GLP-1 system comprise a self-defense mechanism for enhancing ? cell survival to combat lipid overload, which is in part mediated by oxidative stress and inflammation. Twit Text FOAVip Endogenous GLP-1 as a key self-defense molecule against lipotoxicity in pancreatic islets ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25976560 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25976560 #FOAvip English Wikipedia <ref>{{Cite pmid|25976560}}</ref> Endogenous GLP-1 as a key self-defense molecule against lipotoxicity in pancreatic islets #MMPMID25976560 HUANG C; YUAN L; CAO S Int J Mol Med 2015[Jul]; 36 (1): 173-85 PMID25976560show ga The number of pro-? cells is known to increase in response to ? cell injury and these cells then generate glucagon-like peptide-1 (GLP-1), thus attenuating the development of diabetes. The aim of the present study was to further examine the role and the mechanisms responsible for intra-islet GLP-1 production as a self-protective response against lipotoxicity. The levels of the key enzyme, prohormone convertase 1/3 (PC1/3), as well as the synthesis and release of GLP-1 in models of lipotoxicity were measured. Furthermore, islet viability, apoptosis, oxidative stress and inflammation, as well as islet structure were assessed after altering GLP-1 receptor signaling. Both prolonged exposure to palmitate and a high-fat diet facilitated PC1/3 expression, as well as the synthesis and release of GLP-1 induced by ? cell injury and the generation of pro-? cells. Prolonged exposure to palmitate increased reactive oxygen species (ROS) production, and the antioxidant, N-acetylcysteine (NAC), partially prevented the detrimental effects induced by palmitate on ? cells, resulting in decreased GLP-1 levels. Furthermore, the inhibition of GLP-1 receptor (GLP-1R) signaling by treatment with exendin-(9-39) further decreased cell viability, increased cell apoptosis and caused a stronger inhibition of the ? cell-specific transcription factor, pancreatic duodenal homeobox 1 (PDX1). Moreover, treatment with the GLP-1R agonist, liraglutide, normalized islet structure and function, resulting in a decrease in cell death and in the amelioration of ? cell marker expression. Importantly, liraglutide maintained the oxidative balance and decreased inflammatory factor and p65 expression. Overall, our data demonstrate that an increase in the number of pro-? cells and the activation of the intra-islet GLP-1 system comprise a self-defense mechanism for enhancing ? cell survival to combat lipid overload, which is in part mediated by oxidative stress and inflammation. äEndogenous GLP-1 as a key self-defense molecule against lipotoxicity i(epmc).pdf DeepDyve Pubget Overpricing