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10.1038/nature17184 http://scihub22266oqcxt.onion/10.1038/nature17184 C4909121!4909121!26982719     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2016 ; 531 (7595): 528-32 Nephropedia Template TP {{tp|p=26982719|t=2016. PGC1?-dependent NAD biosynthesis links oxidative metabolism to renal protection |pdf=|usr=}}{{26982719}} gab.com Text PGC1 -dependent NAD biosynthesis links oxidative metabolism to renal protection JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=26982719 #FOAvip The energetic burden of continuously concentrating solutes against gradients along the tubule may render the kidney especially vulnerable to ischemia. Indeed, acute kidney injury (AKI) affects 3% of all hospitalized patients.1,2 Here we show that the mitochondrial biogenesis regulator, PGC1?,3,4 is a pivotal determinant of renal recovery from injury by regulating NAD biosynthesis. Following renal ischemia, PGC1??/? mice developed local deficiency of the NAD precursor niacinamide (Nam), marked fat accumulation, and failure to re-establish normal function. Remarkably, exogenous Nam improved local NAD levels, fat accumulation, and renal function in post-ischemic PGC1??/? mice. Inducible tubular transgenic mice (iNephPGC1?) recapitulated the effects of Nam supplementation, including more local NAD and less fat accumulation with better renal function after ischemia. PGC1? coordinately upregulated the enzymes that synthesize NAD de novo from amino acids whereas PGC1? deficiency or AKI attenuated the de novo pathway. Nam enhanced NAD via the enzyme NAMPT and augmented production of the fat breakdown product beta-hydroxybutyrate (?-OHB), leading to increased prostaglandin PGE2, a secreted autocoid that maintains renal function.5 Nam treatment reversed established ischemic AKI and also prevented AKI in an unrelated toxic model. Inhibition of ?-OHB signaling or prostaglandins similarly abolished PGC1?-dependent renoprotection. Given the importance of mitochondrial health in aging and the function of metabolically active organs, the results implicate Nam and NAD as key effectors for achieving PGC1?-dependent stress resistance. Twit Text FOAVip PGC1 -dependent NAD biosynthesis links oxidative metabolism to renal protection ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=26982719 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26982719 #FOAvip English Wikipedia <ref>{{Cite pmid|26982719}}</ref> PGC1?-dependent NAD biosynthesis links oxidative metabolism to renal protection #MMPMID26982719 Tran MT; Zsengeller ZK; Berg AH; Khankin EV; Bhasin MK; Kim W; Clish CB; Stillman IE; Karumanchi SA; Rhee EP; Parikh SM Nature 2016[Mar]; 531 (7595): 528-32 PMID26982719show ga The energetic burden of continuously concentrating solutes against gradients along the tubule may render the kidney especially vulnerable to ischemia. Indeed, acute kidney injury (AKI) affects 3% of all hospitalized patients.1,2 Here we show that the mitochondrial biogenesis regulator, PGC1?,3,4 is a pivotal determinant of renal recovery from injury by regulating NAD biosynthesis. Following renal ischemia, PGC1??/? mice developed local deficiency of the NAD precursor niacinamide (Nam), marked fat accumulation, and failure to re-establish normal function. Remarkably, exogenous Nam improved local NAD levels, fat accumulation, and renal function in post-ischemic PGC1??/? mice. Inducible tubular transgenic mice (iNephPGC1?) recapitulated the effects of Nam supplementation, including more local NAD and less fat accumulation with better renal function after ischemia. PGC1? coordinately upregulated the enzymes that synthesize NAD de novo from amino acids whereas PGC1? deficiency or AKI attenuated the de novo pathway. Nam enhanced NAD via the enzyme NAMPT and augmented production of the fat breakdown product beta-hydroxybutyrate (?-OHB), leading to increased prostaglandin PGE2, a secreted autocoid that maintains renal function.5 Nam treatment reversed established ischemic AKI and also prevented AKI in an unrelated toxic model. Inhibition of ?-OHB signaling or prostaglandins similarly abolished PGC1?-dependent renoprotection. Given the importance of mitochondrial health in aging and the function of metabolically active organs, the results implicate Nam and NAD as key effectors for achieving PGC1?-dependent stress resistance. äPGC1?-dependent NAD biosynthesis links oxidative metabolism to renal p(epmc).pdf DeepDyve Pubget Overpricing