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10.1016/j.ddmod.2013.02.001 http://scihub22266oqcxt.onion/10.1016/j.ddmod.2013.02.001 C5890883!5890883 !29643927     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29643927 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Drug+Discov+Today+Dis+Models 2013 ; 10 (2 ): e101-e109 Nephropedia Template TP {{tp|p=29643927 |t=2013. Mouse Models of ?-cell K(ATP) Channel Dysfunction |pdf=|usr=}}{{29643927 }} gab.com Text Mouse Models of -cell K(ATP) Channel Dysfunction JO: Drug Discov Today Dis Models http://www.kidney.de/pget.php?&tw=1&pmid=29643927 #FOAvip ATP-sensitive K(+) (K(ATP)) channels in pancreatic ?-cells couple glucose metabolism to insulin secretion. Reduced K(ATP) channel activity produces excessive insulin release and hyperinsulinism whereas increased K(ATP) channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of K(ATP) channels, or loss-of-function mutations, are only transiently hypoglycaemic during the neonatal period and often display reduced glucose-stimulated insulin secretion subsequently. Mice with K(ATP) channel gain-of-function mutations are hyperglycaemic and have impaired glucose-stimulated insulin secretion, a phenotype that accurately mimics human diabetes. This review discusses how mice expressing altered K(ATP) channels have provided valuable insight into ?-cell function. Twit Text FOAVip Mouse Models of -cell K(ATP) Channel Dysfunction ????Drug Discov Today Dis Models http://www.kidney.de/pget.php?&tw=1&pmid=29643927 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29643927 #FOAvip English Wikipedia <ref>{{Cite pmid|29643927 }}</ref> Mouse Models of ?-cell K(ATP) Channel Dysfunction #MMPMID29643927 Brereton MF ; Ashcroft FM Drug Discov Today Dis Models 2013[Sum]; 10 (2 ): e101-e109 PMID29643927 show ga ATP-sensitive K(+) (K(ATP)) channels in pancreatic ?-cells couple glucose metabolism to insulin secretion. Reduced K(ATP) channel activity produces excessive insulin release and hyperinsulinism whereas increased K(ATP) channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of K(ATP) channels, or loss-of-function mutations, are only transiently hypoglycaemic during the neonatal period and often display reduced glucose-stimulated insulin secretion subsequently. Mice with K(ATP) channel gain-of-function mutations are hyperglycaemic and have impaired glucose-stimulated insulin secretion, a phenotype that accurately mimics human diabetes. This review discusses how mice expressing altered K(ATP) channels have provided valuable insight into ?-cell function. äMouse Models of ?-cell K(ATP) Channel Dysfunction (epmc).pdf DeepDyve Pubget Overpricing