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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Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Tatulli, Giuseppe" sort="Tatulli, Giuseppe" uniqKey="Tatulli G" first="Giuseppe" last="Tatulli">Giuseppe Tatulli</name><affiliation><nlm:affiliation>Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Maria Cannata, Stefano" sort="Maria Cannata, Stefano" uniqKey="Maria Cannata S" first="Stefano" last="Maria Cannata">Stefano Maria Cannata</name><affiliation><nlm:affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Bernardini, Sergio" sort="Bernardini, Sergio" uniqKey="Bernardini S" first="Sergio" last="Bernardini">Sergio Bernardini</name><affiliation><nlm:affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Aquilano, Katia" sort="Aquilano, Katia" uniqKey="Aquilano K" first="Katia" last="Aquilano">Katia Aquilano</name><affiliation><nlm:affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Ciriolo, Maria R" sort="Ciriolo, Maria R" uniqKey="Ciriolo M" first="Maria R" last="Ciriolo">Maria R. Ciriolo</name><affiliation><nlm:affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="doi">10.1038/srep13091</idno><idno type="RBID">pubmed:26260892</idno><idno type="pmid">26260892</idno><idno type="wicri:Area/PubMed/Corpus">000080</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000080</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Glutathione Decrement Drives Thermogenic Program In Adipose Cells.</title><author><name sortKey="Lettieri Barbato, Daniele" sort="Lettieri Barbato, Daniele" uniqKey="Lettieri Barbato D" first="Daniele" last="Lettieri Barbato">Daniele Lettieri Barbato</name><affiliation><nlm:affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Tatulli, Giuseppe" sort="Tatulli, Giuseppe" uniqKey="Tatulli G" first="Giuseppe" last="Tatulli">Giuseppe Tatulli</name><affiliation><nlm:affiliation>Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Maria Cannata, Stefano" sort="Maria Cannata, Stefano" uniqKey="Maria Cannata S" first="Stefano" last="Maria Cannata">Stefano Maria Cannata</name><affiliation><nlm:affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Bernardini, Sergio" sort="Bernardini, Sergio" uniqKey="Bernardini S" first="Sergio" last="Bernardini">Sergio Bernardini</name><affiliation><nlm:affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Aquilano, Katia" sort="Aquilano, Katia" uniqKey="Aquilano K" first="Katia" last="Aquilano">Katia Aquilano</name><affiliation><nlm:affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Ciriolo, Maria R" sort="Ciriolo, Maria R" uniqKey="Ciriolo M" first="Maria R" last="Ciriolo">Maria R. Ciriolo</name><affiliation><nlm:affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></TEI><pubmed><MedlineCitation Owner="NLM" Status="In-Process"><PMID Version="1">26260892</PMID><DateCreated><Year>2015</Year><Month>08</Month><Day>11</Day></DateCreated><DateRevised><Year>2015</Year><Month>08</Month><Day>14</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Glutathione Decrement Drives Thermogenic Program In Adipose Cells.</ArticleTitle><Pagination><MedlinePgn>13091</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep13091</ELocationID><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></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lettieri Barbato</LastName><ForeName>Daniele</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tatulli</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maria Cannata</LastName><ForeName>Stefano</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bernardini</LastName><ForeName>Sergio</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aquilano</LastName><ForeName>Katia</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ciriolo</LastName><ForeName>Maria R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>1] Dept. Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, 00133 Rome, Italy [2] Scientific Institute for Research Hospitalization and Health Care and Università Telematica San Raffaele Roma, Via di Val Cannuta 247, 00166 Rome, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2010 Dec 17;285(51):39646-54</RefSource><PMID 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