Acute Inhibition of PI3K-PDK1-Akt Pathway Potentiates Insulin Secretion through Upregulation of Newcomer Granule Fusions in Pancreatic β-Cells 英文参考文献.docVIP
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Acute Inhibition of PI3K-PDK1-Akt Pathway Potentiates Insulin Secretion through Upregulation of Newcomer Granule Fusions in Pancreatic β-Cells 英文参考文献
AcuteInhibitionofPI3K-PDK1-AktPathwayPotentiates
InsulinSecretionthroughUpregulationofNewcomer
GranuleFusionsinPancreaticb-Cells
KyotaAoyagi1,MicaOhara-Imaizumi1,ChiyonoNishiwaki1,YokoNakamichi1,KohjiroUeki2,
TakashiKadowaki2,ShinyaNagamatsu1*
1Department of Biochemistry, Kyorin University School of Medicine, Tokyo, Japan, 2Department of Diabetes and Metabolic Diseases, Graduate School of Medicine,
UniversityofTokyo,Tokyo,Japan
Abstract
In glucose-induced insulin secretion from pancreatic b-cells, a population of insulin granules fuses with the plasma
membrane without the typical docking process (newcomer granule fusions), however, its mechanism is unclear. In this
study, we investigated the PI3K signaling pathways involved in the upregulation of newcomer granule fusions. Acute
treatment with the class IA-selective PI3K inhibitors, PIK-75 and PI-103, enhanced the glucose-induced insulin secretion.
Total internal reflection fluorescent microscopy revealed that the PI3K inhibitors increased the fusion events from
newcomergranules.Wedevelopedanewsystemfortransfectionintopancreaticisletsanddemonstratedtheusefulnessof
this system in order for evaluatingthe effect oftransfected genes on theglucose-induced secretionin primary cultured
pancreaticislets.Usingthistransfectionsystemtogetherwithaseriesofconstitutiveactivemutants,weshowedthatthe
PI3K-3-phosphoinositidedependentkinase-1(PDK1)-Aktpathwaymediatedthepotentiationofinsulinsecretion.TheAkt
inhibitor also enhanced the glucose-induced insulin secretion in parallel with the upregulation of newcomer granule
fusions,probablyviaincreasedmotilityofintracellularinsulingranules.ThesedatasuggestthatthePI3K-PDK1-Aktpathway
playsasignificantrole innewcomer granulefusions, probably through analterationofthedynamics oftheintracellular
insulingranules.
Citation:AoyagiK,Ohara-ImaizumiM,NishiwakiC,NakamichiY,UekiK,etal.(2012)AcuteInhibitionofPI3K-PDK1-AktPathwayPotentiatesInsulinSecretion
throughUpregulationofNewcomerGranuleFusion
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