@article{Arvier-2007-ID5,
  title     = {Adenine nucleotide translocator promotes oxidative phosphorylation and mild
               uncoupling in mitochondria after dexamethasone treatment.},
  abstract  = {The composition of the mitochondrial inner membrane and uncoupling protein
               [such as adenine nucleotide translocator ({ANT})] contents are the main
               factors involved in the energy-wasting proton leak. This leak is increased
               by glucocorticoid treatment under nonphosphorylating conditions. The aim of
               this study was to investigate mechanisms involved in glucocorticoid-induced
               proton leak and to evaluate the consequences in more physiological
               conditions (between states 4 and 3). Isolated liver mitochondria, obtained
               from dexamethasone-treated rats (1.5 mg.kg(-1).day(-1)), were studied by
               polarography, Western blotting, and high-performance thin-layer
               chromatography. We confirmed that dexamethasone treatment in rats induces a
               proton leak in state 4 that is associated with an increased {ANT} content,
               although without any change in membrane surface or lipid composition.
               Between states 4 and 3, dexamethasone stimulates {ATP} synthesis by
               increasing both the mitochondrial {ANT} and F1-F0 {ATP} synthase content.
               In conclusion, dexamethasone increases mitochondrial capacity to generate
               {ATP} by modifying {ANT} and {ATP} synthase. The side effect is an
               increased leak in nonphosphorylating conditions.},
  author    = {Arvier, Matthieu and Lagoutte, Laëtitia and Johnson, Gyasi and Dumas,
               Jean-François and Sion, Benoit and Grizard, Genevieve and Malthièry, Yves
               and Simard, Gilles and Ritz, Patrick},
  volume    = {293},
  number    = {5},
  pages     = {E1320--4},
  year      = {2007},
  month     = {11},
  url       = {http://www.pubmed.org/17698987},
  pmid      = {17698987},
  doi       = {10.1152/ajpendo.00138.2007},
  keywords  = {Animals, Mitochondria, Liver, Adenine Nucleotide Translocator 1, Adenosine
               Triphosphate, Cardiolipins, Citrate (si)-Synthase, Dexamethasone,
               Ethanolamines, Glucocorticoids, Male, Membrane Potential, Mitochondrial,
               Mitochondrial Proton-Translocating {ATP}ases, Oxidative Phosphorylation,
               Oxygen Consumption, Phosphatidylcholines, Polarography, Random Allocation,
               Rats, Rats, Sprague-Dawley},
  file      = {FULLTEXT:pdfs/000/000/000000005.pdf:PDF}
}

{"_id":"r7SumMudA4Xfbgc4k","bibbaseid":"arvier-lagoutte-johnson-dumas-sion-grizard-malthiry-simard-etal-adeninenucleotidetranslocatorpromotesoxidativephosphorylationandmilduncouplinginmitochondriaafterdexamethasonetreatment-2007","authorIDs":[],"author_short":["Arvier, M.","Lagoutte, L.","Johnson, G.","Dumas, J.","Sion, B.","Grizard, G.","Malthièry, Y.","Simard, G.","Ritz, P."],"bibdata":{"bibtype":"article","type":"article","title":"Adenine nucleotide translocator promotes oxidative phosphorylation and mild uncoupling in mitochondria after dexamethasone treatment.","abstract":"The composition of the mitochondrial inner membrane and uncoupling protein [such as adenine nucleotide translocator (ANT)] contents are the main factors involved in the energy-wasting proton leak. This leak is increased by glucocorticoid treatment under nonphosphorylating conditions. The aim of this study was to investigate mechanisms involved in glucocorticoid-induced proton leak and to evaluate the consequences in more physiological conditions (between states 4 and 3). Isolated liver mitochondria, obtained from dexamethasone-treated rats (1.5 mg.kg(-1).day(-1)), were studied by polarography, Western blotting, and high-performance thin-layer chromatography. We confirmed that dexamethasone treatment in rats induces a proton leak in state 4 that is associated with an increased ANT content, although without any change in membrane surface or lipid composition. Between states 4 and 3, dexamethasone stimulates ATP synthesis by increasing both the mitochondrial ANT and F1-F0 ATP synthase content. In conclusion, dexamethasone increases mitochondrial capacity to generate ATP by modifying ANT and ATP synthase. The side effect is an increased leak in nonphosphorylating conditions.","author":[{"propositions":[],"lastnames":["Arvier"],"firstnames":["Matthieu"],"suffixes":[]},{"propositions":[],"lastnames":["Lagoutte"],"firstnames":["Laëtitia"],"suffixes":[]},{"propositions":[],"lastnames":["Johnson"],"firstnames":["Gyasi"],"suffixes":[]},{"propositions":[],"lastnames":["Dumas"],"firstnames":["Jean-François"],"suffixes":[]},{"propositions":[],"lastnames":["Sion"],"firstnames":["Benoit"],"suffixes":[]},{"propositions":[],"lastnames":["Grizard"],"firstnames":["Genevieve"],"suffixes":[]},{"propositions":[],"lastnames":["Malthièry"],"firstnames":["Yves"],"suffixes":[]},{"propositions":[],"lastnames":["Simard"],"firstnames":["Gilles"],"suffixes":[]},{"propositions":[],"lastnames":["Ritz"],"firstnames":["Patrick"],"suffixes":[]}],"volume":"293","number":"5","pages":"E1320–4","year":"2007","month":"11","url":"http://www.pubmed.org/17698987","pmid":"17698987","doi":"10.1152/ajpendo.00138.2007","keywords":"Animals, Mitochondria, Liver, Adenine Nucleotide Translocator 1, Adenosine Triphosphate, Cardiolipins, Citrate (si)-Synthase, Dexamethasone, Ethanolamines, Glucocorticoids, Male, Membrane Potential, Mitochondrial, Mitochondrial Proton-Translocating ATPases, Oxidative Phosphorylation, Oxygen Consumption, Phosphatidylcholines, Polarography, Random Allocation, Rats, Rats, Sprague-Dawley","file":"FULLTEXT:pdfs/000/000/000000005.pdf:PDF","bibtex":"@article{Arvier-2007-ID5,\n title = {Adenine nucleotide translocator promotes oxidative phosphorylation and mild\n uncoupling in mitochondria after dexamethasone treatment.},\n abstract = {The composition of the mitochondrial inner membrane and uncoupling protein\n [such as adenine nucleotide translocator ({ANT})] contents are the main\n factors involved in the energy-wasting proton leak. This leak is increased\n by glucocorticoid treatment under nonphosphorylating conditions. The aim of\n this study was to investigate mechanisms involved in glucocorticoid-induced\n proton leak and to evaluate the consequences in more physiological\n conditions (between states 4 and 3). Isolated liver mitochondria, obtained\n from dexamethasone-treated rats (1.5 mg.kg(-1).day(-1)), were studied by\n polarography, Western blotting, and high-performance thin-layer\n chromatography. We confirmed that dexamethasone treatment in rats induces a\n proton leak in state 4 that is associated with an increased {ANT} content,\n although without any change in membrane surface or lipid composition.\n Between states 4 and 3, dexamethasone stimulates {ATP} synthesis by\n increasing both the mitochondrial {ANT} and F1-F0 {ATP} synthase content.\n In conclusion, dexamethasone increases mitochondrial capacity to generate\n {ATP} by modifying {ANT} and {ATP} synthase. The side effect is an\n increased leak in nonphosphorylating conditions.},\n author = {Arvier, Matthieu and Lagoutte, Laëtitia and Johnson, Gyasi and Dumas,\n Jean-François and Sion, Benoit and Grizard, Genevieve and Malthièry, Yves\n and Simard, Gilles and Ritz, Patrick},\n volume = {293},\n number = {5},\n pages = {E1320--4},\n year = {2007},\n month = {11},\n url = {http://www.pubmed.org/17698987},\n pmid = {17698987},\n doi = {10.1152/ajpendo.00138.2007},\n keywords = {Animals, Mitochondria, Liver, Adenine Nucleotide Translocator 1, Adenosine\n Triphosphate, Cardiolipins, Citrate (si)-Synthase, Dexamethasone,\n Ethanolamines, Glucocorticoids, Male, Membrane Potential, Mitochondrial,\n Mitochondrial Proton-Translocating {ATP}ases, Oxidative Phosphorylation,\n Oxygen Consumption, Phosphatidylcholines, Polarography, Random Allocation,\n Rats, Rats, Sprague-Dawley},\n file = {FULLTEXT:pdfs/000/000/000000005.pdf:PDF}\n}\n\n","author_short":["Arvier, M.","Lagoutte, L.","Johnson, G.","Dumas, J.","Sion, B.","Grizard, G.","Malthièry, Y.","Simard, G.","Ritz, P."],"key":"Arvier-2007-ID5","id":"Arvier-2007-ID5","bibbaseid":"arvier-lagoutte-johnson-dumas-sion-grizard-malthiry-simard-etal-adeninenucleotidetranslocatorpromotesoxidativephosphorylationandmilduncouplinginmitochondriaafterdexamethasonetreatment-2007","role":"author","urls":{"Paper":"http://www.pubmed.org/17698987"},"keyword":["Animals","Mitochondria","Liver","Adenine Nucleotide Translocator 1","Adenosine Triphosphate","Cardiolipins","Citrate (si)-Synthase","Dexamethasone","Ethanolamines","Glucocorticoids","Male","Membrane Potential","Mitochondrial","Mitochondrial Proton-Translocating ATPases","Oxidative Phosphorylation","Oxygen Consumption","Phosphatidylcholines","Polarography","Random Allocation","Rats","Rats","Sprague-Dawley"],"downloads":0},"bibtype":"article","biburl":"http://woowoowoo.com/ideas/test.bib","creationDate":"2021-02-10T01:28:56.993Z","downloads":0,"keywords":["animals","mitochondria","liver","adenine nucleotide translocator 1","adenosine triphosphate","cardiolipins","citrate (si)-synthase","dexamethasone","ethanolamines","glucocorticoids","male","membrane potential","mitochondrial","mitochondrial proton-translocating atpases","oxidative phosphorylation","oxygen consumption","phosphatidylcholines","polarography","random allocation","rats","rats","sprague-dawley"],"search_terms":["adenine","nucleotide","translocator","promotes","oxidative","phosphorylation","mild","uncoupling","mitochondria","dexamethasone","treatment","arvier","lagoutte","johnson","dumas","sion","grizard","malthièry","simard","ritz"],"title":"Adenine nucleotide translocator promotes oxidative phosphorylation and mild uncoupling in mitochondria after dexamethasone treatment.","year":2007,"dataSources":["gDKyuywTCAxcaYPT7"]}