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10.1016/j.cmet.2014.06.010 http://scihub22266oqcxt.onion/10.1016/j.cmet.2014.06.010 C4156535!4156535 !25043817     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25043817 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cell+Metab 2014 ; 20 (3 ): 512-25 Nephropedia Template TP {{tp|p=25043817 |t=2014. The PPAR?-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway |pdf=|usr=}}{{25043817 }} gab.com Text The PPAR -FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=25043817 #FOAvip The cJun NH2-terminal kinase (JNK) stress signaling pathway is implicated in the metabolic response to the consumption of a high-fat diet, including the development of obesity and insulin resistance. These metabolic adaptations involve altered liver function. Here, we demonstrate that hepatic JNK potently represses the nuclear hormone receptor peroxisome proliferator-activated receptor ? (PPAR?). Therefore, JNK causes decreased expression of PPAR? target genes that increase fatty acid oxidation and ketogenesis and promote the development of insulin resistance. We show that the PPAR? target gene fibroblast growth factor 21 (Fgf21) plays a key role in this response because disruption of the hepatic PPAR?-FGF21 hormone axis suppresses the metabolic effects of JNK deficiency. This analysis identifies the hepatokine FGF21 as a critical mediator of JNK signaling in the liver. Twit Text FOAVip The PPAR -FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=25043817 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25043817 #FOAvip English Wikipedia <ref>{{Cite pmid|25043817 }}</ref> The PPAR?-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway #MMPMID25043817 Vernia S ; Cavanagh-Kyros J ; Garcia-Haro L ; Sabio G ; Barrett T ; Jung DY ; Kim JK ; Xu J ; Shulha HP ; Garber M ; Gao G ; Davis RJ Cell Metab 2014[Sep]; 20 (3 ): 512-25 PMID25043817 show ga The cJun NH2-terminal kinase (JNK) stress signaling pathway is implicated in the metabolic response to the consumption of a high-fat diet, including the development of obesity and insulin resistance. These metabolic adaptations involve altered liver function. Here, we demonstrate that hepatic JNK potently represses the nuclear hormone receptor peroxisome proliferator-activated receptor ? (PPAR?). Therefore, JNK causes decreased expression of PPAR? target genes that increase fatty acid oxidation and ketogenesis and promote the development of insulin resistance. We show that the PPAR? target gene fibroblast growth factor 21 (Fgf21) plays a key role in this response because disruption of the hepatic PPAR?-FGF21 hormone axis suppresses the metabolic effects of JNK deficiency. This analysis identifies the hepatokine FGF21 as a critical mediator of JNK signaling in the liver. |*MAP Kinase Signaling System [MESH] |Animals [MESH] |Diet, High-Fat/adverse effects [MESH] |Fibroblast Growth Factors/*metabolism [MESH] |Gene Deletion [MESH] |Insulin Resistance [MESH] |Liver/*metabolism [MESH] |MAP Kinase Kinase 4/genetics/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Obesity/etiology/genetics/metabolism [MESH]The PPAR?-FGF21 hormone axis contributes to metabolic regulation by th(epmc).pdf DeepDyve Pubget Overpricing