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http://scihub22266oqcxt.onion/ C4884441!4884441!22414059     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Diabetes+Rev 2012 ; 8 (1): 69-75 Nephropedia Template TP {{tp|p=22414059|t=2012. The Role of Peroxidation of Mitochondrial Membrane Phospholipids in Pancreatic ?-Cell Failure |pdf=|usr=}}{{22414059}} gab.com Text The Role of Peroxidation of Mitochondrial Membrane Phospholipids in Pancreatic -Cell Failure JO: Curr Diabetes Rev http://www.kidney.de/pget.php?&tw=1&pmid=22414059 #FOAvip Type 2 diabetes (T2D) is characterized by peripheral insulin resistance and pancreatic islet ?-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor to ?-cell failure in the pathogenesis of T2D. This review focuses on mechanisms whereby reactive oxygen species (ROS) produced by ?-cell in response to metabolic stress affect mitochondrial structure and function and lead to ?-cell failure. Specifically, ROS oxidize mitochondrial membrane phospholipids such as cardiolipin, which impairs membrane integrity and leads to cytochrome c release and apoptosis. In addition, ROS activate UCP2 via peroxidation of the mitochondrial membrane phospholipids, which results in proton leak leading to reduced ATP synthesis and content in ?-cells ? critical parameters in the regulation of glucose-stimulated insulin secretion. Group VIA Phospholipase A2 (iPLA2?) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA2?-deficiency increases ?-cell mitochondrial susceptibility to injury from ROS and predisposes to development of T2D. Interventions that attenuate the adverse effects of ROS on ?-cell mitochondrial phospholipids may prevent or retard the development of T2D. Twit Text FOAVip The Role of Peroxidation of Mitochondrial Membrane Phospholipids in Pancreatic -Cell Failure ????Curr Diabetes Rev http://www.kidney.de/pget.php?&tw=1&pmid=22414059 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22414059 #FOAvip English Wikipedia <ref>{{Cite pmid|22414059}}</ref> The Role of Peroxidation of Mitochondrial Membrane Phospholipids in Pancreatic ?-Cell Failure #MMPMID22414059 Ma ZA Curr Diabetes Rev 2012[Jan]; 8 (1): 69-75 PMID22414059show ga Type 2 diabetes (T2D) is characterized by peripheral insulin resistance and pancreatic islet ?-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor to ?-cell failure in the pathogenesis of T2D. This review focuses on mechanisms whereby reactive oxygen species (ROS) produced by ?-cell in response to metabolic stress affect mitochondrial structure and function and lead to ?-cell failure. Specifically, ROS oxidize mitochondrial membrane phospholipids such as cardiolipin, which impairs membrane integrity and leads to cytochrome c release and apoptosis. In addition, ROS activate UCP2 via peroxidation of the mitochondrial membrane phospholipids, which results in proton leak leading to reduced ATP synthesis and content in ?-cells ? critical parameters in the regulation of glucose-stimulated insulin secretion. Group VIA Phospholipase A2 (iPLA2?) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA2?-deficiency increases ?-cell mitochondrial susceptibility to injury from ROS and predisposes to development of T2D. Interventions that attenuate the adverse effects of ROS on ?-cell mitochondrial phospholipids may prevent or retard the development of T2D. äThe Role of Peroxidation of Mitochondrial Membrane Phospholipids in Pa(epmc).pdf DeepDyve Pubget Overpricing