An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice.
Identifieur interne : 001720 ( PubMed/Curation ); précédent : 001719; suivant : 001721An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice.
Auteurs : Maria Rohm [Allemagne] ; Michaela Sch Fer [Allemagne] ; Victor Laurent [Allemagne] ; Bilgen Ekim Üstünel [Allemagne] ; Katharina Niopek [Allemagne] ; Carolyn Algire [Allemagne] ; Oksana Hautzinger [Allemagne] ; Tjeerd P. Sijmonsma [Allemagne] ; Annika Zota [Allemagne] ; Dasa Medrikova [Allemagne] ; Natalia S. Pellegata [Allemagne] ; Mikael Ryden [Suède] ; Agné Kulyte [Suède] ; Ingrid Dahlman [Suède] ; Peter Arner [Suède] ; Natasa Petrovic [Suède] ; Barbara Cannon [Suède] ; Ez-Zoubir Amri [France] ; Bruce E. Kemp [Australie] ; Gregory R. Steinberg [Canada] ; Petra Janovska [République tchèque] ; Jan Kopecky [République tchèque] ; Christian Wolfrum [Suisse] ; Matthias Blüher [Allemagne] ; Mauricio Berriel Diaz [Allemagne] ; Stephan Herzig [Allemagne]Source :
- Nature medicine [ 1546-170X ] ; 2016.
Descripteurs français
- KwdFr :
- AMP-Activated Protein Kinases (métabolisme), AMP-Activated Protein Kinases (pharmacologie), Adipocytes blancs (), Adipocytes blancs (métabolisme), Animaux, Cachexie (métabolisme), Cachexie (étiologie), Cellules cultivées, Fragments peptidiques (pharmacologie), Lipogenèse (), Lipolyse (), Métabolisme des lipides (), Protéine-1 de découplage (), Protéine-1 de découplage (métabolisme), Protéines régulatrices de l'apoptose (), Protéines régulatrices de l'apoptose (métabolisme), Souris, Techniques in vitro, Thermogenèse (), Tissu adipeux blanc (), Tissu adipeux blanc (métabolisme), Tumeurs (), Tumeurs (métabolisme).
- MESH :
- métabolisme : AMP-Activated Protein Kinases, Adipocytes blancs, Cachexie, Protéine-1 de découplage, Protéines régulatrices de l'apoptose, Tissu adipeux blanc, Tumeurs.
- pharmacologie : AMP-Activated Protein Kinases, Fragments peptidiques.
- étiologie : Cachexie.
- Adipocytes blancs, Animaux, Cellules cultivées, Lipogenèse, Lipolyse, Métabolisme des lipides, Protéine-1 de découplage, Protéines régulatrices de l'apoptose, Souris, Techniques in vitro, Thermogenèse, Tissu adipeux blanc, Tumeurs.
English descriptors
- KwdEn :
- AMP-Activated Protein Kinases (metabolism), AMP-Activated Protein Kinases (pharmacology), Adipocytes, White (drug effects), Adipocytes, White (metabolism), Adipose Tissue, White (drug effects), Adipose Tissue, White (metabolism), Animals, Apoptosis Regulatory Proteins (drug effects), Apoptosis Regulatory Proteins (metabolism), Cachexia (etiology), Cachexia (metabolism), Cells, Cultured, In Vitro Techniques, Lipid Metabolism (drug effects), Lipogenesis (drug effects), Lipolysis (drug effects), Mice, Neoplasms (complications), Neoplasms (metabolism), Peptide Fragments (pharmacology), Thermogenesis (drug effects), Uncoupling Protein 1 (drug effects), Uncoupling Protein 1 (metabolism).
- MESH :
- chemical , drug effects : Apoptosis Regulatory Proteins, Uncoupling Protein 1.
- chemical , metabolism : AMP-Activated Protein Kinases, Apoptosis Regulatory Proteins, Uncoupling Protein 1.
- chemical , pharmacology : AMP-Activated Protein Kinases, Peptide Fragments.
- complications : Neoplasms.
- drug effects : Adipocytes, White, Adipose Tissue, White, Lipid Metabolism, Lipogenesis, Lipolysis, Thermogenesis.
- etiology : Cachexia.
- metabolism : Adipocytes, White, Adipose Tissue, White, Cachexia, Neoplasms.
- Animals, Cells, Cultured, In Vitro Techniques, Mice.
Abstract
Cachexia represents a fatal energy-wasting syndrome in a large number of patients with cancer that mostly results in a pathological loss of skeletal muscle and adipose tissue. Here we show that tumor cell exposure and tumor growth in mice triggered a futile energy-wasting cycle in cultured white adipocytes and white adipose tissue (WAT), respectively. Although uncoupling protein 1 (Ucp1)-dependent thermogenesis was dispensable for tumor-induced body wasting, WAT from cachectic mice and tumor-cell-supernatant-treated adipocytes were consistently characterized by the simultaneous induction of both lipolytic and lipogenic pathways. Paradoxically, this was accompanied by an inactivated AMP-activated protein kinase (Ampk), which is normally activated in peripheral tissues during states of low cellular energy. Ampk inactivation correlated with its degradation and with upregulation of the Ampk-interacting protein Cidea. Therefore, we developed an Ampk-stabilizing peptide, ACIP, which was able to ameliorate WAT wasting in vitro and in vivo by shielding the Cidea-targeted interaction surface on Ampk. Thus, our data establish the Ucp1-independent remodeling of adipocyte lipid homeostasis as a key event in tumor-induced WAT wasting, and we propose the ACIP-dependent preservation of Ampk integrity in the WAT as a concept in future therapies for cachexia.
DOI: 10.1038/nm.4171
PubMed: 27571348
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<author><name sortKey="Herzig, Stephan" sort="Herzig, Stephan" uniqKey="Herzig S" first="Stephan" last="Herzig">Stephan Herzig</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice.</title>
<author><name sortKey="Rohm, Maria" sort="Rohm, Maria" uniqKey="Rohm M" first="Maria" last="Rohm">Maria Rohm</name>
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<author><name sortKey="Sch Fer, Michaela" sort="Sch Fer, Michaela" uniqKey="Sch Fer M" first="Michaela" last="Sch Fer">Michaela Sch Fer</name>
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<author><name sortKey="Laurent, Victor" sort="Laurent, Victor" uniqKey="Laurent V" first="Victor" last="Laurent">Victor Laurent</name>
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<country xml:lang="fr">Allemagne</country>
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<author><name sortKey="Ustunel, Bilgen Ekim" sort="Ustunel, Bilgen Ekim" uniqKey="Ustunel B" first="Bilgen Ekim" last="Üstünel">Bilgen Ekim Üstünel</name>
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<author><name sortKey="Niopek, Katharina" sort="Niopek, Katharina" uniqKey="Niopek K" first="Katharina" last="Niopek">Katharina Niopek</name>
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<author><name sortKey="Hautzinger, Oksana" sort="Hautzinger, Oksana" uniqKey="Hautzinger O" first="Oksana" last="Hautzinger">Oksana Hautzinger</name>
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<author><name sortKey="Pellegata, Natalia S" sort="Pellegata, Natalia S" uniqKey="Pellegata N" first="Natalia S" last="Pellegata">Natalia S. Pellegata</name>
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<author><name sortKey="Kulyte, Agne" sort="Kulyte, Agne" uniqKey="Kulyte A" first="Agné" last="Kulyte">Agné Kulyte</name>
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<author><name sortKey="Dahlman, Ingrid" sort="Dahlman, Ingrid" uniqKey="Dahlman I" first="Ingrid" last="Dahlman">Ingrid Dahlman</name>
<affiliation wicri:level="1"><nlm:affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm</wicri:regionArea>
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<author><name sortKey="Arner, Peter" sort="Arner, Peter" uniqKey="Arner P" first="Peter" last="Arner">Peter Arner</name>
<affiliation wicri:level="1"><nlm:affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Petrovic, Natasa" sort="Petrovic, Natasa" uniqKey="Petrovic N" first="Natasa" last="Petrovic">Natasa Petrovic</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Cannon, Barbara" sort="Cannon, Barbara" uniqKey="Cannon B" first="Barbara" last="Cannon">Barbara Cannon</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Amri, Ez Zoubir" sort="Amri, Ez Zoubir" uniqKey="Amri E" first="Ez-Zoubir" last="Amri">Ez-Zoubir Amri</name>
<affiliation wicri:level="1"><nlm:affiliation>Université Côte d'Azur, Nice, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Côte d'Azur, Nice</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Kemp, Bruce E" sort="Kemp, Bruce E" uniqKey="Kemp B" first="Bruce E" last="Kemp">Bruce E. Kemp</name>
<affiliation wicri:level="1"><nlm:affiliation>St Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria, Australia.</nlm:affiliation>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>St Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Steinberg, Gregory R" sort="Steinberg, Gregory R" uniqKey="Steinberg G" first="Gregory R" last="Steinberg">Gregory R. Steinberg</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Division of Endocrinology and Metabolism, McMaster University, Hamilton, Ontario, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medicine, Division of Endocrinology and Metabolism, McMaster University, Hamilton, Ontario</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Janovska, Petra" sort="Janovska, Petra" uniqKey="Janovska P" first="Petra" last="Janovska">Petra Janovska</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Kopecky, Jan" sort="Kopecky, Jan" uniqKey="Kopecky J" first="Jan" last="Kopecky">Jan Kopecky</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Wolfrum, Christian" sort="Wolfrum, Christian" uniqKey="Wolfrum C" first="Christian" last="Wolfrum">Christian Wolfrum</name>
<affiliation wicri:level="1"><nlm:affiliation>Swiss Federal Institute of Technology, Institute of Food Nutrition and Health, Schwerzenbach, Switzerland.</nlm:affiliation>
<country xml:lang="fr">Suisse</country>
<wicri:regionArea>Swiss Federal Institute of Technology, Institute of Food Nutrition and Health, Schwerzenbach</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Bluher, Matthias" sort="Bluher, Matthias" uniqKey="Bluher M" first="Matthias" last="Blüher">Matthias Blüher</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, University of Leipzig, Leipzig, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Medicine, University of Leipzig, Leipzig</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Berriel Diaz, Mauricio" sort="Berriel Diaz, Mauricio" uniqKey="Berriel Diaz M" first="Mauricio" last="Berriel Diaz">Mauricio Berriel Diaz</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Herzig, Stephan" sort="Herzig, Stephan" uniqKey="Herzig S" first="Stephan" last="Herzig">Stephan Herzig</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg</wicri:regionArea>
</affiliation>
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<series><title level="j">Nature medicine</title>
<idno type="eISSN">1546-170X</idno>
<imprint><date when="2016" type="published">2016</date>
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<term>AMP-Activated Protein Kinases (pharmacology)</term>
<term>Adipocytes, White (drug effects)</term>
<term>Adipocytes, White (metabolism)</term>
<term>Adipose Tissue, White (drug effects)</term>
<term>Adipose Tissue, White (metabolism)</term>
<term>Animals</term>
<term>Apoptosis Regulatory Proteins (drug effects)</term>
<term>Apoptosis Regulatory Proteins (metabolism)</term>
<term>Cachexia (etiology)</term>
<term>Cachexia (metabolism)</term>
<term>Cells, Cultured</term>
<term>In Vitro Techniques</term>
<term>Lipid Metabolism (drug effects)</term>
<term>Lipogenesis (drug effects)</term>
<term>Lipolysis (drug effects)</term>
<term>Mice</term>
<term>Neoplasms (complications)</term>
<term>Neoplasms (metabolism)</term>
<term>Peptide Fragments (pharmacology)</term>
<term>Thermogenesis (drug effects)</term>
<term>Uncoupling Protein 1 (drug effects)</term>
<term>Uncoupling Protein 1 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>AMP-Activated Protein Kinases (métabolisme)</term>
<term>AMP-Activated Protein Kinases (pharmacologie)</term>
<term>Adipocytes blancs ()</term>
<term>Adipocytes blancs (métabolisme)</term>
<term>Animaux</term>
<term>Cachexie (métabolisme)</term>
<term>Cachexie (étiologie)</term>
<term>Cellules cultivées</term>
<term>Fragments peptidiques (pharmacologie)</term>
<term>Lipogenèse ()</term>
<term>Lipolyse ()</term>
<term>Métabolisme des lipides ()</term>
<term>Protéine-1 de découplage ()</term>
<term>Protéine-1 de découplage (métabolisme)</term>
<term>Protéines régulatrices de l'apoptose ()</term>
<term>Protéines régulatrices de l'apoptose (métabolisme)</term>
<term>Souris</term>
<term>Techniques in vitro</term>
<term>Thermogenèse ()</term>
<term>Tissu adipeux blanc ()</term>
<term>Tissu adipeux blanc (métabolisme)</term>
<term>Tumeurs ()</term>
<term>Tumeurs (métabolisme)</term>
</keywords>
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<term>Uncoupling Protein 1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term>
<term>Apoptosis Regulatory Proteins</term>
<term>Uncoupling Protein 1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>AMP-Activated Protein Kinases</term>
<term>Peptide Fragments</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adipocytes, White</term>
<term>Adipose Tissue, White</term>
<term>Lipid Metabolism</term>
<term>Lipogenesis</term>
<term>Lipolysis</term>
<term>Thermogenesis</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cachexia</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adipocytes, White</term>
<term>Adipose Tissue, White</term>
<term>Cachexia</term>
<term>Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Adipocytes blancs</term>
<term>Cachexie</term>
<term>Protéine-1 de découplage</term>
<term>Protéines régulatrices de l'apoptose</term>
<term>Tissu adipeux blanc</term>
<term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Fragments peptidiques</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Cachexie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cells, Cultured</term>
<term>In Vitro Techniques</term>
<term>Mice</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adipocytes blancs</term>
<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Lipogenèse</term>
<term>Lipolyse</term>
<term>Métabolisme des lipides</term>
<term>Protéine-1 de découplage</term>
<term>Protéines régulatrices de l'apoptose</term>
<term>Souris</term>
<term>Techniques in vitro</term>
<term>Thermogenèse</term>
<term>Tissu adipeux blanc</term>
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<front><div type="abstract" xml:lang="en">Cachexia represents a fatal energy-wasting syndrome in a large number of patients with cancer that mostly results in a pathological loss of skeletal muscle and adipose tissue. Here we show that tumor cell exposure and tumor growth in mice triggered a futile energy-wasting cycle in cultured white adipocytes and white adipose tissue (WAT), respectively. Although uncoupling protein 1 (Ucp1)-dependent thermogenesis was dispensable for tumor-induced body wasting, WAT from cachectic mice and tumor-cell-supernatant-treated adipocytes were consistently characterized by the simultaneous induction of both lipolytic and lipogenic pathways. Paradoxically, this was accompanied by an inactivated AMP-activated protein kinase (Ampk), which is normally activated in peripheral tissues during states of low cellular energy. Ampk inactivation correlated with its degradation and with upregulation of the Ampk-interacting protein Cidea. Therefore, we developed an Ampk-stabilizing peptide, ACIP, which was able to ameliorate WAT wasting in vitro and in vivo by shielding the Cidea-targeted interaction surface on Ampk. Thus, our data establish the Ucp1-independent remodeling of adipocyte lipid homeostasis as a key event in tumor-induced WAT wasting, and we propose the ACIP-dependent preservation of Ampk integrity in the WAT as a concept in future therapies for cachexia.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27571348</PMID>
<DateCreated><Year>2016</Year>
<Month>09</Month>
<Day>26</Day>
</DateCreated>
<DateCompleted><Year>2017</Year>
<Month>08</Month>
<Day>08</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>11</Month>
<Day>16</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1546-170X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>22</Volume>
<Issue>10</Issue>
<PubDate><Year>2016</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>Nature medicine</Title>
<ISOAbbreviation>Nat. Med.</ISOAbbreviation>
</Journal>
<ArticleTitle>An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice.</ArticleTitle>
<Pagination><MedlinePgn>1120-1130</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/nm.4171</ELocationID>
<Abstract><AbstractText>Cachexia represents a fatal energy-wasting syndrome in a large number of patients with cancer that mostly results in a pathological loss of skeletal muscle and adipose tissue. Here we show that tumor cell exposure and tumor growth in mice triggered a futile energy-wasting cycle in cultured white adipocytes and white adipose tissue (WAT), respectively. Although uncoupling protein 1 (Ucp1)-dependent thermogenesis was dispensable for tumor-induced body wasting, WAT from cachectic mice and tumor-cell-supernatant-treated adipocytes were consistently characterized by the simultaneous induction of both lipolytic and lipogenic pathways. Paradoxically, this was accompanied by an inactivated AMP-activated protein kinase (Ampk), which is normally activated in peripheral tissues during states of low cellular energy. Ampk inactivation correlated with its degradation and with upregulation of the Ampk-interacting protein Cidea. Therefore, we developed an Ampk-stabilizing peptide, ACIP, which was able to ameliorate WAT wasting in vitro and in vivo by shielding the Cidea-targeted interaction surface on Ampk. Thus, our data establish the Ucp1-independent remodeling of adipocyte lipid homeostasis as a key event in tumor-induced WAT wasting, and we propose the ACIP-dependent preservation of Ampk integrity in the WAT as a concept in future therapies for cachexia.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rohm</LastName>
<ForeName>Maria</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schäfer</LastName>
<ForeName>Michaela</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Laurent</LastName>
<ForeName>Victor</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Üstünel</LastName>
<ForeName>Bilgen Ekim</ForeName>
<Initials>BE</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Niopek</LastName>
<ForeName>Katharina</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Algire</LastName>
<ForeName>Carolyn</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hautzinger</LastName>
<ForeName>Oksana</ForeName>
<Initials>O</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sijmonsma</LastName>
<ForeName>Tjeerd P</ForeName>
<Initials>TP</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zota</LastName>
<ForeName>Annika</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Medrikova</LastName>
<ForeName>Dasa</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pellegata</LastName>
<ForeName>Natalia S</ForeName>
<Initials>NS</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ryden</LastName>
<ForeName>Mikael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kulyte</LastName>
<ForeName>Agné</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dahlman</LastName>
<ForeName>Ingrid</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Arner</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Lipid Laboratory, Department of Medicine, Karolinska Institute, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Petrovic</LastName>
<ForeName>Natasa</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cannon</LastName>
<ForeName>Barbara</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Amri</LastName>
<ForeName>Ez-Zoubir</ForeName>
<Initials>EZ</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0001-8426-5396</Identifier>
<AffiliationInfo><Affiliation>Université Côte d'Azur, Nice, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre National de la Recherche Scientifique (CNRS), Nice, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kemp</LastName>
<ForeName>Bruce E</ForeName>
<Initials>BE</Initials>
<AffiliationInfo><Affiliation>St Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria, Australia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Mary MacKillop Institute for Health, Research Australian Catholic University, Melbourne, Victoria, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Steinberg</LastName>
<ForeName>Gregory R</ForeName>
<Initials>GR</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Division of Endocrinology and Metabolism, McMaster University, Hamilton, Ontario, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Janovska</LastName>
<ForeName>Petra</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kopecky</LastName>
<ForeName>Jan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wolfrum</LastName>
<ForeName>Christian</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Swiss Federal Institute of Technology, Institute of Food Nutrition and Health, Schwerzenbach, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Blüher</LastName>
<ForeName>Matthias</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Leipzig, Leipzig, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berriel Diaz</LastName>
<ForeName>Mauricio</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Herzig</LastName>
<ForeName>Stephan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Joint Heidelberg-IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Deutsches Zentrum für Diabetesforschung, Neuherberg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>08</Month>
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