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10.1172/JCI92913 http://scihub22266oqcxt.onion/10.1172/JCI92913 C5531395!5531395!28650340     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28650340&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 127 (8): 2941-5 Nephropedia Template TP {{tp|p=28650340|t=ä. Hepatic ?-arrestin 2 is essential for maintaining euglycemia |pdf=|usr=}}{{28650340}} gab.com Text Hepatic -arrestin 2 is essential for maintaining euglycemia JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28650340 #FOAvip An increase in hepatic glucose production (HGP) represents a key feature of type 2 diabetes. This deficiency in metabolic control of glucose production critically depends on enhanced signaling through hepatic glucagon receptors (GCGRs). Here, we have demonstrated that selective inactivation of the GPCR-associated protein ?-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR signaling, leading to striking deficits in glucose homeostasis. However, hepatocyte-specific ?-arrestin 2 deficiency did not affect hepatic insulin sensitivity or ?-adrenergic signaling. Adult mice lacking ?-arrestin 1 selectively in hepatocytes did not show any changes in glucose homeostasis. Importantly, hepatocyte-specific overexpression of ?-arrestin 2 greatly reduced hepatic GCGR signaling and protected mice against the metabolic deficits caused by the consumption of a high-fat diet. Our data support the concept that strategies aimed at enhancing hepatic ?-arrestin 2 activity could prove useful for suppressing HGP for therapeutic purposes. Twit Text FOAVip Hepatic -arrestin 2 is essential for maintaining euglycemia ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28650340 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28650340 #FOAvip English Wikipedia <ref>{{Cite pmid|28650340}}</ref> Hepatic ?-arrestin 2 is essential for maintaining euglycemia #MMPMID28650340 Zhu L; Rossi M; Cui Y; Lee RJ; Sakamoto W; Perry NA; Urs NM; Caron MG; Gurevich VV; Godlewski G; Kunos G; Chen M; Chen W; Wess J J Clin Invest ä[]; 127 (8): 2941-5 PMID28650340show ga An increase in hepatic glucose production (HGP) represents a key feature of type 2 diabetes. This deficiency in metabolic control of glucose production critically depends on enhanced signaling through hepatic glucagon receptors (GCGRs). Here, we have demonstrated that selective inactivation of the GPCR-associated protein ?-arrestin 2 in hepatocytes of adult mice results in greatly increased hepatic GCGR signaling, leading to striking deficits in glucose homeostasis. However, hepatocyte-specific ?-arrestin 2 deficiency did not affect hepatic insulin sensitivity or ?-adrenergic signaling. Adult mice lacking ?-arrestin 1 selectively in hepatocytes did not show any changes in glucose homeostasis. Importantly, hepatocyte-specific overexpression of ?-arrestin 2 greatly reduced hepatic GCGR signaling and protected mice against the metabolic deficits caused by the consumption of a high-fat diet. Our data support the concept that strategies aimed at enhancing hepatic ?-arrestin 2 activity could prove useful for suppressing HGP for therapeutic purposes. äHepatic ?-arrestin 2 is essential for maintaining euglycemia (epmc).pdf DeepDyve Pubget Overpricing