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10.15252/emmm.201708047 http://scihub22266oqcxt.onion/10.15252/emmm.201708047 C5840546!5840546!29343498     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 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2018 ; 10 (3): ä Nephropedia Template TP {{tp|p=29343498|t=2018. The GPR120 agonist TUG?891 promotes metabolic health by stimulating mitochondrial respiration in brown fat |pdf=|usr=}}{{29343498}} gab.com Text The GPR120 agonist TUG 891 promotes metabolic health by stimulating mitochondrial respiration in brown fat JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29343498 #FOAvip Brown adipose tissue (BAT) activation stimulates energy expenditure in human adults, which makes it an attractive target to combat obesity and related disorders. Recent studies demonstrated a role for G protein?coupled receptor 120 (GPR120) in BAT thermogenesis. Here, we investigated the therapeutic potential of GPR120 agonism and addressed GPR120?mediated signaling in BAT. We found that activation of GPR120 by the selective agonist TUG?891 acutely increases fat oxidation and reduces body weight and fat mass in C57Bl/6J mice. These effects coincided with decreased brown adipocyte lipid content and increased nutrient uptake by BAT, confirming increased BAT activity. Consistent with these observations, GPR120 deficiency reduced expression of genes involved in nutrient handling in BAT. Stimulation of brown adipocytes in vitro with TUG?891 acutely induced O2 consumption, through GPR120?dependent and GPR120?independent mechanisms. TUG?891 not only stimulated GPR120 signaling resulting in intracellular calcium release, mitochondrial depolarization, and mitochondrial fission, but also activated UCP1. Collectively, these data suggest that activation of brown adipocytes with the GPR120 agonist TUG?891 is a promising strategy to increase lipid combustion and reduce obesity. Twit Text FOAVip The GPR120 agonist TUG 891 promotes metabolic health by stimulating mitochondrial respiration in brown fat ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29343498 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29343498 #FOAvip English Wikipedia <ref>{{Cite pmid|29343498}}</ref> The GPR120 agonist TUG?891 promotes metabolic health by stimulating mitochondrial respiration in brown fat #MMPMID29343498 Schilperoort M; van Dam AD; Hoeke G; Shabalina IG; Okolo A; Hanyaloglu AC; Dib LH; Mol IM; Caengprasath N; Chan Y; Damak S; Miller AR; Coskun T; Shimpukade B; Ulven T; Kooijman S; Rensen PC; Christian M EMBO Mol Med 2018[Mar]; 10 (3): ä PMID29343498show ga Brown adipose tissue (BAT) activation stimulates energy expenditure in human adults, which makes it an attractive target to combat obesity and related disorders. Recent studies demonstrated a role for G protein?coupled receptor 120 (GPR120) in BAT thermogenesis. Here, we investigated the therapeutic potential of GPR120 agonism and addressed GPR120?mediated signaling in BAT. We found that activation of GPR120 by the selective agonist TUG?891 acutely increases fat oxidation and reduces body weight and fat mass in C57Bl/6J mice. These effects coincided with decreased brown adipocyte lipid content and increased nutrient uptake by BAT, confirming increased BAT activity. Consistent with these observations, GPR120 deficiency reduced expression of genes involved in nutrient handling in BAT. Stimulation of brown adipocytes in vitro with TUG?891 acutely induced O2 consumption, through GPR120?dependent and GPR120?independent mechanisms. TUG?891 not only stimulated GPR120 signaling resulting in intracellular calcium release, mitochondrial depolarization, and mitochondrial fission, but also activated UCP1. Collectively, these data suggest that activation of brown adipocytes with the GPR120 agonist TUG?891 is a promising strategy to increase lipid combustion and reduce obesity. äThe GPR120 agonist TUG?891 promotes metabolic health by stimulating mi(epmc).pdf DeepDyve Pubget Overpricing