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10.1016/j.cmet.2014.06.010

http://scihub22266oqcxt.onion/10.1016/j.cmet.2014.06.010
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C4156535!4156535!25043817
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suck abstract from ncbi


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pmid25043817      Cell+Metab 2014 ; 20 (3): 512-25
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  • 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 PMID25043817show 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?). JNK therefore causes decreased expression of PPAR? target genes that increase fatty acid oxidation / 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.
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