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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       Drug+Discov+Today+Dis+Models 2013 ; 10 (2): e101-9 Nephropedia Template TP {{tp|p=29643927|t=2013. Mouse Models of ?-cell KATP Channel Dysfunction |pdf=|usr=}}{{29643927}} gab.com Text Mouse Models of -cell KATP Channel Dysfunction JO: Drug Discov Today Dis Models http://www.kidney.de/pget.php?&tw=1&pmid=29643927 #FOAvip ATP-sensitive K+ (KATP) channels in pancreatic ?-cells couple glucose metabolism to insulin secretion. Reduced KATP channel activity produces excessive insulin release and hyperinsulinism whereas increased KATP channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of KATP 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 KATP 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 KATP channels have provided valuable insight into ?-cell function. Twit Text FOAVip Mouse Models of -cell KATP 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 KATP Channel Dysfunction #MMPMID29643927 Brereton MF; Ashcroft FM Drug Discov Today Dis Models 2013[Sum]; 10 (2): e101-9 PMID29643927show ga ATP-sensitive K+ (KATP) channels in pancreatic ?-cells couple glucose metabolism to insulin secretion. Reduced KATP channel activity produces excessive insulin release and hyperinsulinism whereas increased KATP channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of KATP 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 KATP 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 KATP channels have provided valuable insight into ?-cell function. äMouse Models of ?-cell KATP Channel Dysfunction (epmc).pdf DeepDyve Pubget Overpricing