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10.1016/j.prostaglandins.2016.07.004 http://scihub22266oqcxt.onion/10.1016/j.prostaglandins.2016.07.004 C5536246!5536246!27418542     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27418542&cmd=llinks): Failed to open stream: HTTP request failed! 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PGC-1 alpha Regulates HO-1 Expression, Mitochondrial Dynamics and Biogenesis: Role of Epoxyeicosatrienoic Acid |pdf=|usr=}}{{27418542}} gab.com Text PGC-1 alpha Regulates HO-1 Expression, Mitochondrial Dynamics and Biogenesis: Role of Epoxyeicosatrienoic Acid JO: Prostaglandins Other Lipid Mediat http://www.kidney.de/pget.php?&tw=1&pmid=27418542 #FOAvip Background/Objectives: Obesity is a risk factor in the development of type 2 diabetes mellitus (DM2), which is associated with increased morbidity and mortality, predominantly as a result of cardiovascular complications. Increased adiposity is a systemic condition characterized by increased oxidative stress (ROS), increased inflammation, inhibition of anti-oxidant genes such as HO-1 and increased degradation of epoxyeicosatrienoic acids (EETs). We previously demonstrated that EETs attenuate mitochondrial ROS. We postulate that EETs increase peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1?), which controls mitochondrial function, oxidative metabolism and induction of HO-1. Subjects/Methods: Cultured murine adipocytes and mice fed a high fat (HF) diet were used to assess functional relationship between EETs, HO-1 and (PGC-1?) using an EET analogue (EET-A) and lentivirus to knock down the PPARGC1A gene. Results: EET-A increased PGC-1? and HO-1 in cultured adipocytes and increased the expression of genes involved in thermogenesis and adipocyte browning (UCP1 and PRDM16, respectively). PGC-1? knockdown prevented EET-A-induced HO-1expression, suggesting that PGC-1? is upstream of HO-1. MRI data obtained from fat tissues showed that EET-A administration to mice on a HF diet significantly reduced total body fat content, subcutaneous and visceral fat deposits and reduced the VAT: SAT ratio. Moreover EET-A normalized the VO2 and RQ (VCO2/VO2) in mice fed a HF diet, an effect that was completely prevented in PGC-1? deficient mice. In addition, EET-A increased mitochondrial biogenesis and function as measured by OPA1, MnSOD, Mfn1, Mfn2, and SIRT3, an effect that was inhibited by knockdown of PGC-1?. Conclusion: Taken together, our findings show that EET-A increased PGC-1? thereby increasing mitochondrial viability, increased fusion potential thereby providing metabolic protection and increased VO2 consumption in HF-induced obesity in mice, thus demonstrating that the EET-mediated increase in HO-1 levels require PGC-1? expression. Twit Text FOAVip PGC-1 alpha Regulates HO-1 Expression, Mitochondrial Dynamics and Biogenesis: Role of Epoxyeicosatrienoic Acid ????Prostaglandins Other Lipid Mediat http://www.kidney.de/pget.php?&tw=1&pmid=27418542 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27418542 #FOAvip English Wikipedia <ref>{{Cite pmid|27418542}}</ref> PGC-1 alpha Regulates HO-1 Expression, Mitochondrial Dynamics and Biogenesis: Role of Epoxyeicosatrienoic Acid #MMPMID27418542 Singh SP; Schragenheim J; Cao J; Abraham NG; Bellner L Prostaglandins Other Lipid Mediat 2016[Sep]; 125 (ä): 8-18 PMID27418542show ga Background/Objectives: Obesity is a risk factor in the development of type 2 diabetes mellitus (DM2), which is associated with increased morbidity and mortality, predominantly as a result of cardiovascular complications. Increased adiposity is a systemic condition characterized by increased oxidative stress (ROS), increased inflammation, inhibition of anti-oxidant genes such as HO-1 and increased degradation of epoxyeicosatrienoic acids (EETs). We previously demonstrated that EETs attenuate mitochondrial ROS. We postulate that EETs increase peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1?), which controls mitochondrial function, oxidative metabolism and induction of HO-1. Subjects/Methods: Cultured murine adipocytes and mice fed a high fat (HF) diet were used to assess functional relationship between EETs, HO-1 and (PGC-1?) using an EET analogue (EET-A) and lentivirus to knock down the PPARGC1A gene. Results: EET-A increased PGC-1? and HO-1 in cultured adipocytes and increased the expression of genes involved in thermogenesis and adipocyte browning (UCP1 and PRDM16, respectively). PGC-1? knockdown prevented EET-A-induced HO-1expression, suggesting that PGC-1? is upstream of HO-1. MRI data obtained from fat tissues showed that EET-A administration to mice on a HF diet significantly reduced total body fat content, subcutaneous and visceral fat deposits and reduced the VAT: SAT ratio. Moreover EET-A normalized the VO2 and RQ (VCO2/VO2) in mice fed a HF diet, an effect that was completely prevented in PGC-1? deficient mice. In addition, EET-A increased mitochondrial biogenesis and function as measured by OPA1, MnSOD, Mfn1, Mfn2, and SIRT3, an effect that was inhibited by knockdown of PGC-1?. Conclusion: Taken together, our findings show that EET-A increased PGC-1? thereby increasing mitochondrial viability, increased fusion potential thereby providing metabolic protection and increased VO2 consumption in HF-induced obesity in mice, thus demonstrating that the EET-mediated increase in HO-1 levels require PGC-1? expression. äPGC-1 alpha Regulates HO-1 Expression, Mitochondrial Dynamics and Biog(epmc).pdf DeepDyve Pubget Overpricing