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10.1038/s41598-017-01603-9 http://scihub22266oqcxt.onion/10.1038/s41598-017-01603-9 C5431091!5431091 !28469249     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28469249 &cmd=llinks): Failed to open stream: HTTP request failed! 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Protectin DX ameliorates palmitate- or high-fat diet-induced insulin resistance and inflammation through an AMPK-PPAR?-dependent pathway in mice |pdf=|usr=}}{{28469249 }} gab.com Text Protectin DX ameliorates palmitate- or high-fat diet-induced insulin resistance and inflammation through an AMPK-PPAR -dependent pathway in mice JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28469249 #FOAvip Protectin DX (PDX), a double lipoxygenase derivative of docosahexaenoic acid, has been reported to attenuate inflammation and insulin resistance. In the current study, we explored the effects of PDX on hyperlipidemia-induced insulin resistance and inflammation through AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor ? (PPAR?). PDX attenuated the impairment of insulin receptor substrate 1/Akt-mediated insulin signaling in palmitate-treated differentiated C2C12 cells and soleus skeletal muscle of HFD-fed mice. Furthermore, PDX treatment significantly ameliorated HFD-induced weight gain and improved glucose tolerance in mice. Nuclear factor kB nuclear translocation, inhibitory kB? phosphorylation, and expression of proinflammatory cytokines were markedly attenuated by PDX in both in vitro and in vivo models. PDX treatment markedly augmented AMPK phosphorylation and PPAR? expression in C2C12 cells and in skeletal muscle of mice. AMPK- and PPAR?-specific siRNAs significantly abrogated the suppressive effects of PDX on palmitate-induced insulin resistance and inflammation. Furthermore, PDX markedly stimulated the expression of genes related to fatty acid oxidation. These effects of PDX were significantly suppressed by AMPK and PPAR? siRNAs. In conclusion, our results demonstrate that PDX ameliorates insulin resistance and inflammation and stimulates fatty acid oxidation through AMPK- and PPAR?-mediated pathways in skeletal muscle. Twit Text FOAVip Protectin DX ameliorates palmitate- or high-fat diet-induced insulin resistance and inflammation through an AMPK-PPAR -dependent pathway in mice ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28469249 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28469249 #FOAvip English Wikipedia <ref>{{Cite pmid|28469249 }}</ref> Protectin DX ameliorates palmitate- or high-fat diet-induced insulin resistance and inflammation through an AMPK-PPAR?-dependent pathway in mice #MMPMID28469249 Jung TW ; Kim HC ; Abd El-Aty AM ; Jeong JH Sci Rep 2017[May]; 7 (1 ): 1397 PMID28469249 show ga Protectin DX (PDX), a double lipoxygenase derivative of docosahexaenoic acid, has been reported to attenuate inflammation and insulin resistance. In the current study, we explored the effects of PDX on hyperlipidemia-induced insulin resistance and inflammation through AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor ? (PPAR?). PDX attenuated the impairment of insulin receptor substrate 1/Akt-mediated insulin signaling in palmitate-treated differentiated C2C12 cells and soleus skeletal muscle of HFD-fed mice. Furthermore, PDX treatment significantly ameliorated HFD-induced weight gain and improved glucose tolerance in mice. Nuclear factor kB nuclear translocation, inhibitory kB? phosphorylation, and expression of proinflammatory cytokines were markedly attenuated by PDX in both in vitro and in vivo models. PDX treatment markedly augmented AMPK phosphorylation and PPAR? expression in C2C12 cells and in skeletal muscle of mice. AMPK- and PPAR?-specific siRNAs significantly abrogated the suppressive effects of PDX on palmitate-induced insulin resistance and inflammation. Furthermore, PDX markedly stimulated the expression of genes related to fatty acid oxidation. These effects of PDX were significantly suppressed by AMPK and PPAR? siRNAs. In conclusion, our results demonstrate that PDX ameliorates insulin resistance and inflammation and stimulates fatty acid oxidation through AMPK- and PPAR?-mediated pathways in skeletal muscle. |*Insulin Resistance [MESH] |AMP-Activated Protein Kinases/*metabolism [MESH] |Animals [MESH] |Anti-Inflammatory Agents, Non-Steroidal/administration & dosage [MESH] |Cells, Cultured [MESH] |Diet, High-Fat [MESH] |Docosahexaenoic Acids/*administration & dosage [MESH] |Hypoglycemic Agents/administration & dosage [MESH] |Inflammation/chemically induced/*metabolism/prevention & control [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Muscle, Skeletal/drug effects/metabolism [MESH] |PPAR alpha/*metabolism [MESH] |Palmitates/administration & dosage [MESH]Protectin DX ameliorates palmitate- or high-fat diet-induced insulin r(epmc).pdf DeepDyve Pubget Overpricing