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10.1016/j.cmet.2016.04.003 http://scihub22266oqcxt.onion/10.1016/j.cmet.2016.04.003 C4873618!4873618!27133129     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Metab 2016 ; 23 (5): 821-36 Nephropedia Template TP {{tp|p=27133129|t=2016. Chronic Activation of ?2 AMPK Induces Obesity and Reduces ? Cell Function |pdf=|usr=}}{{27133129}} gab.com Text Chronic Activation of 2 AMPK Induces Obesity and Reduces Cell Function JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=27133129 #FOAvip Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK ?2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease. Twit Text FOAVip Chronic Activation of 2 AMPK Induces Obesity and Reduces Cell Function ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=27133129 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27133129 #FOAvip English Wikipedia <ref>{{Cite pmid|27133129}}</ref> Chronic Activation of ?2 AMPK Induces Obesity and Reduces ? Cell Function #MMPMID27133129 Yavari A; Stocker C; Ghaffari S; Wargent E; Steeples V; Czibik G; Pinter K; Bellahcene M; Woods A; Martínez de Morentin P; Cansell C; Lam B; Chuster A; Petkevicius K; Nguyen-Tu MS; Martinez-Sanchez A; Pullen T; Oliver P; Stockenhuber A; Nguyen C; Lazdam M; O?Dowd J; Harikumar P; Tóth M; Beall C; Kyriakou T; Parnis J; Sarma D; Katritsis G; Wortmann D; Harper A; Brown L; Willows R; Gandra S; Poncio V; de Oliveira Figueiredo M; Qi N; Peirson S; McCrimmon R; Gereben B; Tretter L; Fekete C; Redwood C; Yeo G; Heisler L; Rutter G; Smith M; Withers D; Carling D; Sternick E; Arch J; Cawthorne M; Watkins H; Ashrafian H Cell Metab 2016[May]; 23 (5): 821-36 PMID27133129show ga Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK ?2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease. äChronic Activation of ?2 AMPK Induces Obesity and Reduces ? Cell Funct(epmc).pdf DeepDyve Pubget Overpricing