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10.1038/srep10741 http://scihub22266oqcxt.onion/10.1038/srep10741 C4454144!4454144!26038839     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2015 ; 5 (ä): ä Nephropedia Template TP {{tp|p=26038839|t=2015. CD38-mediated Ca2+ signaling contributes to glucagon-induced hepatic gluconeogenesis |pdf=|usr=}}{{26038839}} gab.com Text CD38-mediated Ca2+ signaling contributes to glucagon-induced hepatic gluconeogenesis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26038839 #FOAvip CD38 is a multifunctional enzyme for the synthesis of Ca2+ second messengers. Glucagon promotes hepatic glucose production through Ca2+ signaling in the fasting condition. In this study, we investigated the role of CD38 in the glucagon signaling of hepatocytes. Here, we show that glucagon induces cyclic ADP-ribose (cADPR) production and sustained Ca2+ increases via CD38 in hepatocytes. 8-Br-cADPR, an antagonistic cADPR analog, completely blocked glucagon-induced Ca2+ increases and phosphorylation of cAMP response element-binding protein (CREB). Moreover, glucagon-induced sustained Ca2+ signals and translocation of CREB-regulated transcription coactivator 2 to the nucleus were absent and glucagon-induced glucose production and expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (Pck1) are remarkably reduced in hepatocytes from CD38?/? mice. Furthermore, in the fasting condition, CD38?/? mice have decreased blood glucose and hepatic expression of G6Pase and Pck1 compared to wild type mice. Our data suggest that CD38/cADPR-mediated Ca2+ signals play a key role in glucagon-induced gluconeogenesis in hepatocytes, and that the signal pathway has significant clinical implications in metabolic diseases, including type 2 diabetes. Twit Text FOAVip CD38-mediated Ca2+ signaling contributes to glucagon-induced hepatic gluconeogenesis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26038839 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26038839 #FOAvip English Wikipedia <ref>{{Cite pmid|26038839}}</ref> CD38-mediated Ca2+ signaling contributes to glucagon-induced hepatic gluconeogenesis #MMPMID26038839 Rah SY; Kim UH Sci Rep 2015[]; 5 (ä): ä PMID26038839show ga CD38 is a multifunctional enzyme for the synthesis of Ca2+ second messengers. Glucagon promotes hepatic glucose production through Ca2+ signaling in the fasting condition. In this study, we investigated the role of CD38 in the glucagon signaling of hepatocytes. Here, we show that glucagon induces cyclic ADP-ribose (cADPR) production and sustained Ca2+ increases via CD38 in hepatocytes. 8-Br-cADPR, an antagonistic cADPR analog, completely blocked glucagon-induced Ca2+ increases and phosphorylation of cAMP response element-binding protein (CREB). Moreover, glucagon-induced sustained Ca2+ signals and translocation of CREB-regulated transcription coactivator 2 to the nucleus were absent and glucagon-induced glucose production and expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (Pck1) are remarkably reduced in hepatocytes from CD38?/? mice. Furthermore, in the fasting condition, CD38?/? mice have decreased blood glucose and hepatic expression of G6Pase and Pck1 compared to wild type mice. Our data suggest that CD38/cADPR-mediated Ca2+ signals play a key role in glucagon-induced gluconeogenesis in hepatocytes, and that the signal pathway has significant clinical implications in metabolic diseases, including type 2 diabetes. äCD38-mediated Ca2+ signaling contributes to glucagon-induced hepatic g(epmc).pdf DeepDyve Pubget Overpricing