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10.1172/JCI94505 http://scihub22266oqcxt.onion/10.1172/JCI94505 C5785257!5785257!29337301     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 128 (2): 746-59 Nephropedia Template TP {{tp|p=29337301|t=ä. Hepatic Gi signaling regulates whole-body glucose homeostasis |pdf=|usr=}}{{29337301}} gab.com Text Hepatic Gi signaling regulates whole-body glucose homeostasis JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=29337301 #FOAvip An increase in hepatic glucose production (HGP) is a key feature of type 2 diabetes. Excessive signaling through hepatic Gs?linked glucagon receptors critically contributes to pathologically elevated HGP. Here, we tested the hypothesis that this metabolic impairment can be counteracted by enhancing hepatic Gi signaling. Specifically, we used a chemogenetic approach to selectively activate Gi-type G proteins in mouse hepatocytes in vivo. Unexpectedly, activation of hepatic Gi signaling triggered a pronounced increase in HGP and severely impaired glucose homeostasis. Moreover, increased Gi signaling stimulated glucose release in human hepatocytes. A lack of functional Gi-type G proteins in hepatocytes reduced blood glucose levels and protected mice against the metabolic deficits caused by the consumption of a high-fat diet. Additionally, we delineated a signaling cascade that links hepatic Gi signaling to ROS production, JNK activation, and a subsequent increase in HGP. Taken together, our data support the concept that drugs able to block hepatic Gi?coupled GPCRs may prove beneficial as antidiabetic drugs. Twit Text FOAVip Hepatic Gi signaling regulates whole-body glucose homeostasis ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=29337301 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29337301 #FOAvip English Wikipedia <ref>{{Cite pmid|29337301}}</ref> Hepatic Gi signaling regulates whole-body glucose homeostasis #MMPMID29337301 Rossi M; Zhu L; McMillin SM; Pydi SP; Jain S; Wang L; Cui Y; Lee RJ; Cohen AH; Kaneto H; Birnbaum MJ; Ma Y; Rotman Y; Liu J; Cyphert TJ; Finkel T; McGuinness OP; Wess J J Clin Invest ä[]; 128 (2): 746-59 PMID29337301show ga An increase in hepatic glucose production (HGP) is a key feature of type 2 diabetes. Excessive signaling through hepatic Gs?linked glucagon receptors critically contributes to pathologically elevated HGP. Here, we tested the hypothesis that this metabolic impairment can be counteracted by enhancing hepatic Gi signaling. Specifically, we used a chemogenetic approach to selectively activate Gi-type G proteins in mouse hepatocytes in vivo. Unexpectedly, activation of hepatic Gi signaling triggered a pronounced increase in HGP and severely impaired glucose homeostasis. Moreover, increased Gi signaling stimulated glucose release in human hepatocytes. A lack of functional Gi-type G proteins in hepatocytes reduced blood glucose levels and protected mice against the metabolic deficits caused by the consumption of a high-fat diet. Additionally, we delineated a signaling cascade that links hepatic Gi signaling to ROS production, JNK activation, and a subsequent increase in HGP. Taken together, our data support the concept that drugs able to block hepatic Gi?coupled GPCRs may prove beneficial as antidiabetic drugs. äHepatic Gi signaling regulates whole-body glucose homeostasis (epmc).pdf DeepDyve Pubget Overpricing