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10.1152/ajpregu.00520.2013 http://scihub22266oqcxt.onion/10.1152/ajpregu.00520.2013 C3962623!3962623!24477542     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Regul+Integr+Comp+Physiol 2014 ; 306 (7): R447-56 Nephropedia Template TP {{tp|p=24477542|t=2014. Supraoptic oxytocin and vasopressin neurons function as glucose and metabolic sensors |pdf=|usr=}}{{24477542}} gab.com Text Supraoptic oxytocin and vasopressin neurons function as glucose and metabolic sensors JO: Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24477542 #FOAvip Neurons in the supraoptic nuclei (SON) produce oxytocin and vasopressin and express insulin receptors (InsR) and glucokinase. Since oxytocin is an anorexigenic agent and glucokinase and InsR are hallmarks of cells that function as glucose and/or metabolic sensors, we evaluated the effect of glucose, insulin, and their downstream effector ATP-sensitive potassium (KATP) channels on calcium signaling in SON neurons and on oxytocin and vasopressin release from explants of the rat hypothalamo-neurohypophyseal system. We also evaluated the effect of blocking glucokinase and phosphatidylinositol 3 kinase (PI3K; mediates insulin-induced mobilization of glucose transporter, GLUT4) on responses to glucose and insulin. Glucose and insulin increased intracellular calcium ([Ca2+]i). The responses were glucokinase and PI3K dependent, respectively. Insulin and glucose alone increased vasopressin release (P < 0.002). Oxytocin release was increased by glucose in the presence of insulin. The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P ? 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P ? 0.002). Inactivating KATP channels with 200 nM glibenclamide increased oxytocin and vasopressin release (OT: P < 0.003; VP: P < 0.05). These results suggest that insulin activation of PI3K increases glucokinase-mediated ATP production inducing closure of KATP channels, opening of voltage-sensitive calcium channels, and stimulation of oxytocin and vasopressin release. The findings are consistent with SON oxytocin and vasopressin neurons functioning as glucose and ?metabolic? sensors to participate in appetite regulation. Twit Text FOAVip Supraoptic oxytocin and vasopressin neurons function as glucose and metabolic sensors ????Am J Physiol Regul Integr Comp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24477542 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24477542 #FOAvip English Wikipedia <ref>{{Cite pmid|24477542}}</ref> Supraoptic oxytocin and vasopressin neurons function as glucose and metabolic sensors #MMPMID24477542 Song Z; Levin BE; Stevens W; Sladek CD Am J Physiol Regul Integr Comp Physiol 2014[Apr]; 306 (7): R447-56 PMID24477542show ga Neurons in the supraoptic nuclei (SON) produce oxytocin and vasopressin and express insulin receptors (InsR) and glucokinase. Since oxytocin is an anorexigenic agent and glucokinase and InsR are hallmarks of cells that function as glucose and/or metabolic sensors, we evaluated the effect of glucose, insulin, and their downstream effector ATP-sensitive potassium (KATP) channels on calcium signaling in SON neurons and on oxytocin and vasopressin release from explants of the rat hypothalamo-neurohypophyseal system. We also evaluated the effect of blocking glucokinase and phosphatidylinositol 3 kinase (PI3K; mediates insulin-induced mobilization of glucose transporter, GLUT4) on responses to glucose and insulin. Glucose and insulin increased intracellular calcium ([Ca2+]i). The responses were glucokinase and PI3K dependent, respectively. Insulin and glucose alone increased vasopressin release (P < 0.002). Oxytocin release was increased by glucose in the presence of insulin. The oxytocin (OT) and vasopressin (VP) responses to insulin+glucose were blocked by the glucokinase inhibitor alloxan (4 mM; P ? 0.002) and the PI3K inhibitor wortmannin (50 nM; OT: P = 0.03; VP: P ? 0.002). Inactivating KATP channels with 200 nM glibenclamide increased oxytocin and vasopressin release (OT: P < 0.003; VP: P < 0.05). These results suggest that insulin activation of PI3K increases glucokinase-mediated ATP production inducing closure of KATP channels, opening of voltage-sensitive calcium channels, and stimulation of oxytocin and vasopressin release. The findings are consistent with SON oxytocin and vasopressin neurons functioning as glucose and ?metabolic? sensors to participate in appetite regulation. äSupraoptic oxytocin and vasopressin neurons function as glucose and me(epmc).pdf DeepDyve Pubget Overpricing