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10.1080/10715762.2016.1239017 http://scihub22266oqcxt.onion/10.1080/10715762.2016.1239017 C5466075!5466075!27646831     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Free+Radic+Res 2016 ; 50 (10): 1080-8 Nephropedia Template TP {{tp|p=27646831|t=2016. The regulatory Roles of O-GlcNAcylation in mitochondrial Homeostasis and metabolic Syndrome |pdf=|usr=}}{{27646831}} gab.com Text The regulatory Roles of O-GlcNAcylation in mitochondrial Homeostasis and metabolic Syndrome JO: Free Radic Res http://www.kidney.de/pget.php?&tw=1&pmid=27646831 #FOAvip Nutrients excess is one of the leading causes of metabolic syndrome globally. Protein post-translational O-GlcNAc modification has been recognized as an essential nutrient sensor of the cell. Emerging studies suggest that O-GlcNAcylation lies at the core linking nutritional stress to insulin resistance. Mitochondria are the major site for ATP production in most eukaryotes. Mitochondrial dysfunction and oxidative stress have long been considered as an important mechanism underlying insulin resistance. The metabolic process is under the influence of environmental and nutritional factors, thus sensing and transducing nutritional signals sit at the pivot of metabolism control. For a long time little was known about O-GlcNAcylation within mitochondria since mitochondrial O-GlcNAcylation was regarded rare. Recent findings have demonstrated that O-GlcNAcylation is widely spread among mitochondrial proteins, and that mitochondrial function and oxidative stress both can be regulated by O-GlcNAcylation, particularly under diabetic circumstances. Twit Text FOAVip The regulatory Roles of O-GlcNAcylation in mitochondrial Homeostasis and metabolic Syndrome ????Free Radic Res http://www.kidney.de/pget.php?&tw=1&pmid=27646831 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27646831 #FOAvip English Wikipedia <ref>{{Cite pmid|27646831}}</ref> The regulatory Roles of O-GlcNAcylation in mitochondrial Homeostasis and metabolic Syndrome #MMPMID27646831 Zhao L; Feng Z; Yang X; Liu J Free Radic Res 2016[Oct]; 50 (10): 1080-8 PMID27646831show ga Nutrients excess is one of the leading causes of metabolic syndrome globally. Protein post-translational O-GlcNAc modification has been recognized as an essential nutrient sensor of the cell. Emerging studies suggest that O-GlcNAcylation lies at the core linking nutritional stress to insulin resistance. Mitochondria are the major site for ATP production in most eukaryotes. Mitochondrial dysfunction and oxidative stress have long been considered as an important mechanism underlying insulin resistance. The metabolic process is under the influence of environmental and nutritional factors, thus sensing and transducing nutritional signals sit at the pivot of metabolism control. For a long time little was known about O-GlcNAcylation within mitochondria since mitochondrial O-GlcNAcylation was regarded rare. Recent findings have demonstrated that O-GlcNAcylation is widely spread among mitochondrial proteins, and that mitochondrial function and oxidative stress both can be regulated by O-GlcNAcylation, particularly under diabetic circumstances. äThe regulatory Roles of O-GlcNAcylation in mitochondrial Homeostasis a(epmc).pdf DeepDyve Pubget Overpricing