Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation
Identifieur interne : 000001 ( Pmc/Corpus ); précédent : 000000; suivant : 000002Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation
Auteurs : D. Lettieri Barbato ; K. Aquilano ; S. Baldelli ; S M Cannata ; S. Bernardini ; G. Rotilio ; M R CirioloSource :
- Cell Death and Differentiation [ 1350-9047 ] ; 2013.
Abstract
The nutrient-sensing lipolytic enzyme adipose triglyceride lipase (ATGL) has a key role in adipose tissue function, and alterations in its activity have been implicated in many age-related metabolic disorders. In adipose tissue reduced blood vessel density is related to hypoxia state, cell death and inflammation. Here we demonstrate that adipocytes of poorly vascularized enlarged visceral adipose tissue (i.e. adipose tissue of old mice) suffer from limited nutrient delivery. In particular, nutrient starvation elicits increased activity of mitochondrial proline oxidase/dehydrogenase (POX/PRODH) that is causal in triggering a ROS-dependent induction of ATGL. We demonstrate that ATGL promotes the expression of genes related to mitochondrial oxidative metabolism (peroxisome proliferator-activated receptor-
Url:
DOI: 10.1038/cdd.2013.137
PubMed: 24096872
PubMed Central: 3857628
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PMC:3857628Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>The nutrient-sensing lipolytic enzyme adipose triglyceride lipase (ATGL) has a key role in adipose tissue function, and alterations in its activity have been implicated in many age-related metabolic disorders. In adipose tissue reduced blood vessel density is related to hypoxia state, cell death and inflammation. Here we demonstrate that adipocytes of poorly vascularized enlarged visceral adipose tissue (i.e. adipose tissue of old mice) suffer from limited nutrient delivery. In particular, nutrient starvation elicits increased activity of mitochondrial proline oxidase/dehydrogenase (POX/PRODH) that is causal in triggering a ROS-dependent induction of ATGL. We demonstrate that ATGL promotes the expression of genes related to mitochondrial oxidative metabolism (peroxisome proliferator-activated receptor-<italic>α</italic>
, peroxisome proliferator-activated receptor-γ coactivator-1<italic>α</italic>
), thus setting a metabolic switch towards fat utilization that supplies energy to starved adipocytes and prevents cell death, as well as adipose tissue inflammation. Taken together, these results identify ATGL as a stress resistance mediator in adipocytes, restraining visceral adipose tissue dysfunction typical of age-related metabolic disorders.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Death Differ</journal-id>
<journal-id journal-id-type="iso-abbrev">Cell Death Differ</journal-id>
<journal-title-group><journal-title>Cell Death and Differentiation</journal-title>
</journal-title-group>
<issn pub-type="ppub">1350-9047</issn>
<issn pub-type="epub">1476-5403</issn>
<publisher><publisher-name>Nature Publishing Group</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24096872</article-id>
<article-id pub-id-type="pmc">3857628</article-id>
<article-id pub-id-type="pii">cdd2013137</article-id>
<article-id pub-id-type="doi">10.1038/cdd.2013.137</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Paper</subject>
</subj-group>
</article-categories>
<title-group><article-title>Proline oxidase–adipose triglyceride lipase pathway restrains adipose cell death and tissue inflammation</article-title>
<alt-title alt-title-type="running">ATGL restrains death in starved adipocytes</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Lettieri Barbato</surname>
<given-names>D</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="author-notes" rid="note1"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Aquilano</surname>
<given-names>K</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="author-notes" rid="note1"><sup>4</sup>
</xref>
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<contrib contrib-type="author"><name><surname>Baldelli</surname>
<given-names>S</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cannata</surname>
<given-names>S M</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bernardini</surname>
<given-names>S</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rotilio</surname>
<given-names>G</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ciriolo</surname>
<given-names>M R</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff3">3</xref>
<xref ref-type="corresp" rid="caf1">*</xref>
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<aff id="aff1"><label>1</label>
<institution>Department of Biology, University of Rome Tor Vergata</institution>
, via della Ricerca Scientifica, 00133 Rome,<country>Italy</country>
</aff>
<aff id="aff2"><label>2</label>
<institution>Università Telematica San Raffaele Roma</institution>
, via di Val Cannuta 247, 00166 Rome,<country>Italy</country>
</aff>
<aff id="aff3"><label>3</label>
<institution>IRCCS San Raffaele</institution>
, via di Val Cannuta 247, 00166 Rome,<country>Italy</country>
</aff>
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<author-notes><corresp id="caf1"><label>*</label>
<institution>Department of Biology, University of Rome Tor Vergata</institution>
, via della Ricerca Scientifica, 00133 Rome, <country>Italy</country>
. Tel: +390672594369; Fax: +390672594311; E-mail: <email>ciriolo@bio.uniroma2.it</email>
</corresp>
<fn fn-type="present-address" id="note1"><label>4</label>
<p>These authors contributed equally to this work.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>01</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>04</day>
<month>10</month>
<year>2013</year>
</pub-date>
<volume>21</volume>
<issue>1</issue>
<fpage>113</fpage>
<lpage>123</lpage>
<history><date date-type="received"><day>05</day>
<month>06</month>
<year>2013</year>
</date>
<date date-type="rev-recd"><day>22</day>
<month>08</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>29</day>
<month>08</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2014 Macmillan Publishers Limited</copyright-statement>
<copyright-year>2014</copyright-year>
<copyright-holder>Macmillan Publishers Limited</copyright-holder>
</permissions>
<abstract><p>The nutrient-sensing lipolytic enzyme adipose triglyceride lipase (ATGL) has a key role in adipose tissue function, and alterations in its activity have been implicated in many age-related metabolic disorders. In adipose tissue reduced blood vessel density is related to hypoxia state, cell death and inflammation. Here we demonstrate that adipocytes of poorly vascularized enlarged visceral adipose tissue (i.e. adipose tissue of old mice) suffer from limited nutrient delivery. In particular, nutrient starvation elicits increased activity of mitochondrial proline oxidase/dehydrogenase (POX/PRODH) that is causal in triggering a ROS-dependent induction of ATGL. We demonstrate that ATGL promotes the expression of genes related to mitochondrial oxidative metabolism (peroxisome proliferator-activated receptor-<italic>α</italic>
, peroxisome proliferator-activated receptor-γ coactivator-1<italic>α</italic>
), thus setting a metabolic switch towards fat utilization that supplies energy to starved adipocytes and prevents cell death, as well as adipose tissue inflammation. Taken together, these results identify ATGL as a stress resistance mediator in adipocytes, restraining visceral adipose tissue dysfunction typical of age-related metabolic disorders.</p>
</abstract>
<kwd-group><kwd>ageing</kwd>
<kwd>adipocytes</kwd>
<kwd>lipid signalling</kwd>
<kwd>mitochondrial metabolism</kwd>
<kwd>reactive oxygen species</kwd>
<kwd>starvation</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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