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10.2337/db14-0508 http://scihub22266oqcxt.onion/10.2337/db14-0508 C5703413!5703413!25338814     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 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Diabetes 2015 ; 64 (2): 360-9 Nephropedia Template TP {{tp|p=25338814|t=2015. Methotrexate promotes glucose uptake and lipid oxidation in skeletal muscle via AMPK activation |pdf=|usr=}}{{25338814}} gab.com Text Methotrexate promotes glucose uptake and lipid oxidation in skeletal muscle via AMPK activation JO: Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=25338814 #FOAvip Methotrexate (MTX) is a widely used anti-cancer and anti-rheumatic drug that has been postulated to protect against metabolic risk factors associated with type 2 diabetes mellitus, although the mechanism remains unknown. MTX inhibits 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase / inosine monophosphate cyclohydrolase (ATIC) and thereby slows down the metabolism of ZMP and its precursor AICAR, which is a pharmacological AMPK activator. We explored whether MTX promotes AMPK activation in cultured myotubes and isolated skeletal muscle. We found MTX markedly reduced the threshold for AICAR-induced AMPK activation, and potentiated glucose uptake and lipid oxidation. Gene silencing of the MTX target ATIC activated AMPK and stimulated lipid oxidation in cultured myotubes. Furthermore, MTX activated AMPK in wild-type HEK-293 cells. These effects were abolished in skeletal muscle lacking the muscle-specific, ZMP-sensitive AMPK-?3 subunit and in HEK-293 cells expressing a ZMP-insensitive mutant AMPK-?2 subunit. Collectively, our findings underscore a role for AMPK as a direct molecular link between MTX and energy metabolism in skeletal muscle. Co-therapy with AICAR and MTX could represent a novel strategy to treat metabolic disorders and overcome current limitations of AICAR mono-therapy. Twit Text FOAVip Methotrexate promotes glucose uptake and lipid oxidation in skeletal muscle via AMPK activation ????Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=25338814 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25338814 #FOAvip English Wikipedia <ref>{{Cite pmid|25338814}}</ref> Methotrexate promotes glucose uptake and lipid oxidation in skeletal muscle via AMPK activation #MMPMID25338814 Pirkmajer S; Kulkarni SS; Tom RZ; Fyffe FA; Hawley SA; Hardie DG; Zierath JR; Chibalin AV Diabetes 2015[Feb]; 64 (2): 360-9 PMID25338814show ga Methotrexate (MTX) is a widely used anti-cancer and anti-rheumatic drug that has been postulated to protect against metabolic risk factors associated with type 2 diabetes mellitus, although the mechanism remains unknown. MTX inhibits 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase / inosine monophosphate cyclohydrolase (ATIC) and thereby slows down the metabolism of ZMP and its precursor AICAR, which is a pharmacological AMPK activator. We explored whether MTX promotes AMPK activation in cultured myotubes and isolated skeletal muscle. We found MTX markedly reduced the threshold for AICAR-induced AMPK activation, and potentiated glucose uptake and lipid oxidation. Gene silencing of the MTX target ATIC activated AMPK and stimulated lipid oxidation in cultured myotubes. Furthermore, MTX activated AMPK in wild-type HEK-293 cells. These effects were abolished in skeletal muscle lacking the muscle-specific, ZMP-sensitive AMPK-?3 subunit and in HEK-293 cells expressing a ZMP-insensitive mutant AMPK-?2 subunit. Collectively, our findings underscore a role for AMPK as a direct molecular link between MTX and energy metabolism in skeletal muscle. Co-therapy with AICAR and MTX could represent a novel strategy to treat metabolic disorders and overcome current limitations of AICAR mono-therapy. äMethotrexate promotes glucose uptake and lipid oxidation in skeletal m(epmc).pdf DeepDyve Pubget Overpricing