Glutathione Decrement Drives Thermogenic Program In Adipose Cells.
Identifieur interne : 000080 ( PubMed/Corpus ); précédent : 000079; suivant : 000081Glutathione Decrement Drives Thermogenic Program In Adipose Cells.
Auteurs : Daniele Lettieri Barbato ; Giuseppe Tatulli ; Stefano Maria Cannata ; Sergio Bernardini ; Katia Aquilano ; Maria R. CirioloSource :
- Scientific reports [ 2045-2322 ] ; 2015.
Abstract
Adipose tissue metabolically adapts to external stimuli. We demonstrate that the induction of the thermogenic program in white adipocytes, through cold exposure in mice or in vitro adrenergic stimulation, is accompanied by a decrease in the intracellular content of glutathione (GSH). Moreover, the treatment with a GSH depleting agent, buthionine sulfoximine (BSO), recapitulates the effect of cold exposure resulting in the induction of thermogenic program. In particular, BSO treatment leads to enhanced uncoupling respiration as demonstrated by increased expression of thermogenic genes (e.g. Ucp1, Ppargc1a), augmented oxygen consumption and decreased mitochondrial transmembrane potential. Buffering GSH decrement by pre-treatment with GSH ester prevents the up-regulation of typical markers of uncoupling respiration. We demonstrate that FoxO1 activation is responsible for the conversion of white adipocytes into a brown phenotype as the "browning" effects of BSO are completely abrogated in cells down-regulating FoxO1. In mice, the BSO-mediated up-regulation of uncoupling genes results in weight loss that is at least in part ascribed to adipose tissue mass reduction. The induction of thermogenic program has been largely proposed to counteract obesity-related diseases. Based on these findings, we propose GSH as a novel therapeutic target to increase energy expenditure in adipocytes.
DOI: 10.1038/srep13091
PubMed: 26260892
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pubmed:26260892Le document en format XML
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<author><name sortKey="Ciriolo, Maria R" sort="Ciriolo, Maria R" uniqKey="Ciriolo M" first="Maria R" last="Ciriolo">Maria R. Ciriolo</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Glutathione Decrement Drives Thermogenic Program In Adipose Cells.</title>
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<author><name sortKey="Bernardini, Sergio" sort="Bernardini, Sergio" uniqKey="Bernardini S" first="Sergio" last="Bernardini">Sergio Bernardini</name>
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<author><name sortKey="Aquilano, Katia" sort="Aquilano, Katia" uniqKey="Aquilano K" first="Katia" last="Aquilano">Katia Aquilano</name>
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<front><div type="abstract" xml:lang="en">Adipose tissue metabolically adapts to external stimuli. We demonstrate that the induction of the thermogenic program in white adipocytes, through cold exposure in mice or in vitro adrenergic stimulation, is accompanied by a decrease in the intracellular content of glutathione (GSH). Moreover, the treatment with a GSH depleting agent, buthionine sulfoximine (BSO), recapitulates the effect of cold exposure resulting in the induction of thermogenic program. In particular, BSO treatment leads to enhanced uncoupling respiration as demonstrated by increased expression of thermogenic genes (e.g. Ucp1, Ppargc1a), augmented oxygen consumption and decreased mitochondrial transmembrane potential. Buffering GSH decrement by pre-treatment with GSH ester prevents the up-regulation of typical markers of uncoupling respiration. We demonstrate that FoxO1 activation is responsible for the conversion of white adipocytes into a brown phenotype as the "browning" effects of BSO are completely abrogated in cells down-regulating FoxO1. In mice, the BSO-mediated up-regulation of uncoupling genes results in weight loss that is at least in part ascribed to adipose tissue mass reduction. The induction of thermogenic program has been largely proposed to counteract obesity-related diseases. Based on these findings, we propose GSH as a novel therapeutic target to increase energy expenditure in adipocytes.</div>
</front>
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<ArticleTitle>Glutathione Decrement Drives Thermogenic Program In Adipose Cells.</ArticleTitle>
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<Abstract><AbstractText>Adipose tissue metabolically adapts to external stimuli. We demonstrate that the induction of the thermogenic program in white adipocytes, through cold exposure in mice or in vitro adrenergic stimulation, is accompanied by a decrease in the intracellular content of glutathione (GSH). Moreover, the treatment with a GSH depleting agent, buthionine sulfoximine (BSO), recapitulates the effect of cold exposure resulting in the induction of thermogenic program. In particular, BSO treatment leads to enhanced uncoupling respiration as demonstrated by increased expression of thermogenic genes (e.g. Ucp1, Ppargc1a), augmented oxygen consumption and decreased mitochondrial transmembrane potential. Buffering GSH decrement by pre-treatment with GSH ester prevents the up-regulation of typical markers of uncoupling respiration. We demonstrate that FoxO1 activation is responsible for the conversion of white adipocytes into a brown phenotype as the "browning" effects of BSO are completely abrogated in cells down-regulating FoxO1. In mice, the BSO-mediated up-regulation of uncoupling genes results in weight loss that is at least in part ascribed to adipose tissue mass reduction. The induction of thermogenic program has been largely proposed to counteract obesity-related diseases. Based on these findings, we propose GSH as a novel therapeutic target to increase energy expenditure in adipocytes.</AbstractText>
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<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2010 Dec 17;285(51):39646-54</RefSource>
<PMID Version="1">20937819</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Clin Endocrinol (Oxf). 2015 Apr;82(4):467-74</RefSource>
<PMID Version="1">25287317</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Mol Biol Lett. 2011 Mar;16(1):149-61</RefSource>
<PMID Version="1">21225471</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Cell Physiol. 2011 Aug;226(8):2016-24</RefSource>
<PMID Version="1">21520053</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2011 Sep 7;14(3):324-38</RefSource>
<PMID Version="1">21907139</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2011 Oct 5;14(4):478-90</RefSource>
<PMID Version="1">21982708</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Obesity (Silver Spring). 2011 Dec;19(12):2429-32</RefSource>
<PMID Version="1">21959341</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Toxicol Appl Pharmacol. 2011 Dec 15;257(3):338-48</RefSource>
<PMID Version="1">21967773</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2012 Jan;26(1):363-75</RefSource>
<PMID Version="1">21940996</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nature. 2012 Jan 26;481(7382):463-8</RefSource>
<PMID Version="1">22237023</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Genes Dev. 2012 Feb 1;26(3):271-81</RefSource>
<PMID Version="1">22302939</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2012 Mar 7;15(3):382-94</RefSource>
<PMID Version="1">22405073</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Diabetes. 2012 Sep;4(3):196</RefSource>
<PMID Version="1">22372821</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Rev Endocrinol. 2014 Jan;10(1):24-36</RefSource>
<PMID Version="1">24146030</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 1999 Dec;27(11-12):1208-18</RefSource>
<PMID Version="1">10641713</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 2001 Jun 1;30(11):1191-212</RefSource>
<PMID Version="1">11368918</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biofactors. 2003;17(1-4):307-14</RefSource>
<PMID Version="1">12897452</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Diabetologia. 2004 May;47(5):794-805</RefSource>
<PMID Version="1">15127200</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Appl Physiol (1985). 1988 Jan;64(1):115-9</RefSource>
<PMID Version="1">3356628</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 1992 Oct;13(4):325-40</RefSource>
<PMID Version="1">1398216</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Arch Biochem Biophys. 1995 Feb 1;316(2):941-9</RefSource>
<PMID Version="1">7864653</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Bull Cancer. 1994 Dec;81 Suppl 2:55s-61s</RefSource>
<PMID Version="1">7727860</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Natl Cancer Inst. 1997 Dec 3;89(23):1789-96</RefSource>
<PMID Version="1">9392620</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 1998 Jul 15;102(2):412-20</RefSource>
<PMID Version="1">9664083</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci Methods. 2006 Apr 15;152(1-2):136-43</RefSource>
<PMID Version="1">16253339</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 May 5;281(18):12682-7</RefSource>
<PMID Version="1">16377639</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>FEBS Lett. 2006 Nov 27;580(27):6391-8</RefSource>
<PMID Version="1">17098232</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2007 Aug 24;282(34):24660-9</RefSource>
<PMID Version="1">17584738</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Diabetes. 2008 Mar;57(3):563-76</RefSource>
<PMID Version="1">18162510</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 2008 Apr 15;44(8):1592-8</RefSource>
<PMID Version="1">18249196</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 2009 Apr 9;360(15):1509-17</RefSource>
<PMID Version="1">19357406</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Protoc. 2009;4(11):1582-90</RefSource>
<PMID Version="1">19816421</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2010 Feb;1797(2):285-95</RefSource>
<PMID Version="1">19925774</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2010 Mar 5;285(10):7153-64</RefSource>
<PMID Version="1">20028987</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Science. 2010 May 28;328(5982):1113-4</RefSource>
<PMID Version="1">20448151</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Science. 2010 May 28;328(5982):1158-61</RefSource>
<PMID Version="1">20448152</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Differentiation. 2010 Jul;80(1):31-9</RefSource>
<PMID Version="1">20471742</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Adv Nutr. 2013 Jan;4(1):62-6</RefSource>
<PMID Version="1">23319124</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2013 May;1831(5):924-33</RefSource>
<PMID Version="1">23376222</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2013 May;1831(5):986-1003</RefSource>
<PMID Version="1">23454373</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2013 May;1831(5):950-9</RefSource>
<PMID Version="1">23454374</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Diabetes. 2013 Jun;62(6):1783-90</RefSource>
<PMID Version="1">23704519</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2013 Jul 23;110(30):12480-5</RefSource>
<PMID Version="1">23818608</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2013 Sep 3;18(3):333-40</RefSource>
<PMID Version="1">24011069</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2013;8(9):e73680</RefSource>
<PMID Version="1">24040023</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Death Dis. 2013;4:e861</RefSource>
<PMID Version="1">24136225</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2013 Oct;1302:11-23</RefSource>
<PMID Version="1">24111875</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Death Differ. 2014 Jan;21(1):113-23</RefSource>
<PMID Version="1">24096872</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Obes Rev. 2014 Feb;15(2):92-106</RefSource>
<PMID Version="1">24165204</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>FEBS J. 2014 Feb;281(3):739-49</RefSource>
<PMID Version="1">24237962</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2014 Mar;1842(3):358-69</RefSource>
<PMID Version="1">23688783</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Vet Med Sci. 2014 Jan;76(1):57-64</RefSource>
<PMID Version="1">24065084</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Endocrinol. 2014 Jul;222(1):R25-38</RefSource>
<PMID Version="1">24781257</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2014 Sep 2;20(3):433-47</RefSource>
<PMID Version="1">25043816</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nature. 2014 Sep 4;513(7516):100-4</RefSource>
<PMID Version="1">25043053</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Differentiation. 2014 Jun;87(5):183-92</RefSource>
<PMID Version="1">25130315</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Int J Biochem Cell Biol. 2011 Jan;43(1):163-9</RefSource>
<PMID Version="1">21056687</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
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