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10.1074/jbc.M114.567271 http://scihub22266oqcxt.onion/10.1074/jbc.M114.567271 C4110255!4110255 !24928508     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24928508 &cmd=llinks): Failed to open stream: HTTP request failed! 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Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK) |pdf=|usr=}}{{24928508 }} gab.com Text Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK) JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=24928508 #FOAvip Metformin is a first-line antidiabetic agent taken by 150 million people across the world every year, yet its mechanism remains only partially understood and controversial. It was proposed that suppression of glucose production in hepatocytes by metformin is AMPK-independent; however, unachievably high concentrations of metformin were employed in these studies. In the current study, we find that metformin, via an AMP-activated protein kinase (AMPK)-dependent mechanism, suppresses glucose production and gluconeogenic gene expression in primary hepatocytes at concentrations found in the portal vein of animals (60-80 ?M). Metformin also inhibits gluconeogenic gene expression in the liver of mice administered orally with metformin. Furthermore, the cAMP-PKA pathway negatively regulates AMPK activity through phosphorylation at Ser-485/497 on the ? subunit, which in turn reduces net phosphorylation at Thr-172. Because diabetic patients often have hyperglucagonemia, AMPK? phosphorylation at Ser-485/497 is a therapeutic target to improve metformin efficacy. Twit Text FOAVip Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK) ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=24928508 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24928508 #FOAvip English Wikipedia <ref>{{Cite pmid|24928508 }}</ref> Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK) #MMPMID24928508 Cao J ; Meng S ; Chang E ; Beckwith-Fickas K ; Xiong L ; Cole RN ; Radovick S ; Wondisford FE ; He L J Biol Chem 2014[Jul]; 289 (30 ): 20435-46 PMID24928508 show ga Metformin is a first-line antidiabetic agent taken by 150 million people across the world every year, yet its mechanism remains only partially understood and controversial. It was proposed that suppression of glucose production in hepatocytes by metformin is AMPK-independent; however, unachievably high concentrations of metformin were employed in these studies. In the current study, we find that metformin, via an AMP-activated protein kinase (AMPK)-dependent mechanism, suppresses glucose production and gluconeogenic gene expression in primary hepatocytes at concentrations found in the portal vein of animals (60-80 ?M). Metformin also inhibits gluconeogenic gene expression in the liver of mice administered orally with metformin. Furthermore, the cAMP-PKA pathway negatively regulates AMPK activity through phosphorylation at Ser-485/497 on the ? subunit, which in turn reduces net phosphorylation at Thr-172. Because diabetic patients often have hyperglucagonemia, AMPK? phosphorylation at Ser-485/497 is a therapeutic target to improve metformin efficacy. |AMP-Activated Protein Kinases/*metabolism [MESH] |Animals [MESH] |Cells, Cultured [MESH] |Cyclic AMP-Dependent Protein Kinases/metabolism [MESH] |Dose-Response Relationship, Drug [MESH] |Gene Expression Regulation/drug effects [MESH] |Gluconeogenesis/*drug effects [MESH] |Glucose/*biosynthesis [MESH] |Hepatocytes/cytology/*metabolism [MESH] |Hypoglycemic Agents/*pharmacology [MESH] |Metformin/*pharmacology [MESH]Low concentrations of metformin suppress glucose production in hepatoc(epmc).pdf DeepDyve Pubget Overpricing