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10.1038/s41467-018-04353-y http://scihub22266oqcxt.onion/10.1038/s41467-018-04353-y C5958052!5958052!29773801     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       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=29773801|t=2018. LRRC8/VRAC anion channels enhance ?-cell glucose sensing and insulin secretion |pdf=|usr=}}{{29773801}} gab.com Text LRRC8/VRAC anion channels enhance -cell glucose sensing and insulin secretion JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29773801 #FOAvip Glucose homeostasis depends critically on insulin that is secreted by pancreatic ?-cells. Serum glucose, which is directly sensed by ?-cells, stimulates depolarization- and Ca2+-dependent exocytosis of insulin granules. Here we show that pancreatic islets prominently express LRRC8A and LRRC8D, subunits of volume-regulated VRAC anion channels. Hypotonicity- or glucose-induced ?-cell swelling elicits canonical LRRC8A-dependent VRAC currents that depolarize ?-cells to an extent that causes electrical excitation. Glucose-induced excitation and Ca2+ responses are delayed in onset, but not abolished, in ?-cells lacking the essential VRAC subunit LRRC8A. Whereas Lrrc8a disruption does not affect tolbutamide- or high-K+-induced insulin secretion from pancreatic islets, it reduces first-phase glucose-induced insulin secretion. Mice lacking VRAC in ?-cells have normal resting serum glucose levels but impaired glucose tolerance. We propose that opening of LRRC8/VRAC channels increases glucose sensitivity and insulin secretion of ?-cells synergistically with KATP closure. Neurotransmitter-permeable LRRC8D-containing VRACs might have additional roles in autocrine/paracrine signaling within islets. Twit Text FOAVip LRRC8/VRAC anion channels enhance -cell glucose sensing and insulin secretion ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29773801 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29773801 #FOAvip English Wikipedia <ref>{{Cite pmid|29773801}}</ref> LRRC8/VRAC anion channels enhance ?-cell glucose sensing and insulin secretion #MMPMID29773801 Stuhlmann T; Planells-Cases R; Jentsch TJ Nat Commun 2018[]; 9 (ä): ä PMID29773801show ga Glucose homeostasis depends critically on insulin that is secreted by pancreatic ?-cells. Serum glucose, which is directly sensed by ?-cells, stimulates depolarization- and Ca2+-dependent exocytosis of insulin granules. Here we show that pancreatic islets prominently express LRRC8A and LRRC8D, subunits of volume-regulated VRAC anion channels. Hypotonicity- or glucose-induced ?-cell swelling elicits canonical LRRC8A-dependent VRAC currents that depolarize ?-cells to an extent that causes electrical excitation. Glucose-induced excitation and Ca2+ responses are delayed in onset, but not abolished, in ?-cells lacking the essential VRAC subunit LRRC8A. Whereas Lrrc8a disruption does not affect tolbutamide- or high-K+-induced insulin secretion from pancreatic islets, it reduces first-phase glucose-induced insulin secretion. Mice lacking VRAC in ?-cells have normal resting serum glucose levels but impaired glucose tolerance. We propose that opening of LRRC8/VRAC channels increases glucose sensitivity and insulin secretion of ?-cells synergistically with KATP closure. Neurotransmitter-permeable LRRC8D-containing VRACs might have additional roles in autocrine/paracrine signaling within islets. äLRRC8/VRAC anion channels enhance ?-cell glucose sensing and insulin s(epmc).pdf DeepDyve Pubget Overpricing