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1000 Titel
  • Glucose substitution prolongs maintenance of energy homeostasis and lifespan of telomere dysfunctional mice
1000 Autor/in
  1. Missios, Pavlos |
  2. Zhou, Yuan |
  3. http://orcid.org/0000-0003-1152-9930 |
  4. von Figura, Guido |
  5. Wegner, Andre |
  6. Chakkarappan, Sundaram Reddy |
  7. Binz, Tina |
  8. Gompf, Anne |
  9. Hartleben, Götz |
  10. Burkhalter, Martin D. |
  11. Wulff, Veronika |
  12. Günes, Cagatay |
  13. Sattler, Rui Wang |
  14. Song, Zhangfa |
  15. Illig, Thomas |
  16. Klaus, Susanne |
  17. Böhm, Bernhard O. |
  18. Wenz, Tina |
  19. Hiller, Karsten |
  20. Rudolph, K. Lenhard |
1000 Erscheinungsjahr 2014
1000 LeibnizOpen
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2014-09-18
1000 Erschienen in
1000 Quellenangabe
  • 5: 4924
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2014
1000 Lizenz
1000 Verlagsversion
  • https://dx.doi.org/10.1038/ncomms5924 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199114/ |
1000 Ergänzendes Material
  • https://www.nature.com/articles/ncomms5924#supplementary-information |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • DNA damage and telomere dysfunction shorten organismal lifespan. Here we show that oral glucose administration at advanced age increases health and lifespan of telomere dysfunctional mice. The study reveals that energy consumption increases in telomere dysfunctional cells resulting in enhanced glucose metabolism both in glycolysis and in the tricarboxylic acid cycle at organismal level. In ageing telomere dysfunctional mice, normal diet provides insufficient amounts of glucose thus leading to impaired energy homeostasis, catabolism, suppression of IGF-1/mTOR signalling, suppression of mitochondrial biogenesis and tissue atrophy. A glucose-enriched diet reverts these defects by activating glycolysis, mitochondrial biogenesis and oxidative glucose metabolism. The beneficial effects of glucose substitution on mitochondrial function and glucose metabolism are blocked by mTOR inhibition but mimicked by IGF-1 application. Together, these results provide the first experimental evidence that telomere dysfunction enhances the requirement of glucose substitution for the maintenance of energy homeostasis and IGF-1/mTOR-dependent mitochondrial biogenesis in ageing tissues.
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/creator/TWlzc2lvcywgUGF2bG9z|https://frl.publisso.de/adhoc/creator/WmhvdSwgWXVhbg==|http://orcid.org/0000-0003-1152-9930|https://frl.publisso.de/adhoc/creator/dm9uIEZpZ3VyYSwgR3VpZG8=|https://frl.publisso.de/adhoc/creator/V2VnbmVyLCBBbmRyZQ==|https://frl.publisso.de/adhoc/creator/Q2hha2thcmFwcGFuLCBTdW5kYXJhbSBSZWRkeQ==|https://frl.publisso.de/adhoc/creator/QmlueiwgVGluYQ==|https://frl.publisso.de/adhoc/creator/R29tcGYsIEFubmU=|https://frl.publisso.de/adhoc/creator/SGFydGxlYmVuLCBHw7Z0eg==|https://frl.publisso.de/adhoc/creator/QnVya2hhbHRlciwgTWFydGluIEQu|https://frl.publisso.de/adhoc/creator/V3VsZmYsIFZlcm9uaWth|https://frl.publisso.de/adhoc/creator/R8O8bmVzLCBDYWdhdGF5|https://frl.publisso.de/adhoc/creator/U2F0dGxlciwgUnVpIFdhbmc=|https://frl.publisso.de/adhoc/creator/U29uZywgWmhhbmdmYQ==|https://frl.publisso.de/adhoc/creator/SWxsaWcsIFRob21hcw==|https://frl.publisso.de/adhoc/creator/S2xhdXMsIFN1c2FubmU=|https://frl.publisso.de/adhoc/creator/QsO2aG0sIEJlcm5oYXJkIE8u|https://frl.publisso.de/adhoc/creator/V2VueiwgVGluYQ==|https://frl.publisso.de/adhoc/creator/SGlsbGVyLCBLYXJzdGVu|https://frl.publisso.de/adhoc/creator/UnVkb2xwaCwgSy4gTGVuaGFyZA==
1000 Label
1000 Förderer
  1. German Research Foundation (DFG) |
  2. European Union |
  3. Federal Ministry of Education and Research (BMBF) |
  4. Leibniz Association |
  5. Research Training Group of Molecular Diabetology and Endocrinology in Medicine at Ulm University |
  6. International Graduate School in Molecular Medicine Ulm |
  7. German Federal and State Governments |
  8. Fonds National de la Recherche (FNR), Luxembourg |
  9. Metabolomics Junior Research Group, Luxembourg |
1000 Fördernummer
  1. RU-745-12; WE 4108/3-1
  2. ERC-2012-AdG 323136
  3. 315894; 01GM1113C
  4. -
  5. GRK 1041
  6. -
  7. GSC270
  8. 1328318
  9. -
1000 Förderprogramm
  1. Emmy-Noether-Program
  2. -
  3. GerontoSys—SyStaR; mitoNET- German Network for Mitochondrial Diseases
  4. -
  5. -
  6. -
  7. -
  8. AFR grant
  9. ATTRACT program
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer German Research Foundation (DFG) |
    1000 Förderprogramm Emmy-Noether-Program
    1000 Fördernummer RU-745-12; WE 4108/3-1
  2. 1000 joinedFunding-child
    1000 Förderer European Union |
    1000 Förderprogramm -
    1000 Fördernummer ERC-2012-AdG 323136
  3. 1000 joinedFunding-child
    1000 Förderer Federal Ministry of Education and Research (BMBF) |
    1000 Förderprogramm GerontoSys—SyStaR; mitoNET- German Network for Mitochondrial Diseases
    1000 Fördernummer 315894; 01GM1113C
  4. 1000 joinedFunding-child
    1000 Förderer Leibniz Association |
    1000 Förderprogramm -
    1000 Fördernummer -
  5. 1000 joinedFunding-child
    1000 Förderer Research Training Group of Molecular Diabetology and Endocrinology in Medicine at Ulm University |
    1000 Förderprogramm -
    1000 Fördernummer GRK 1041
  6. 1000 joinedFunding-child
    1000 Förderer International Graduate School in Molecular Medicine Ulm |
    1000 Förderprogramm -
    1000 Fördernummer -
  7. 1000 joinedFunding-child
    1000 Förderer German Federal and State Governments |
    1000 Förderprogramm -
    1000 Fördernummer GSC270
  8. 1000 joinedFunding-child
    1000 Förderer Fonds National de la Recherche (FNR), Luxembourg |
    1000 Förderprogramm AFR grant
    1000 Fördernummer 1328318
  9. 1000 joinedFunding-child
    1000 Förderer Metabolomics Junior Research Group, Luxembourg |
    1000 Förderprogramm ATTRACT program
    1000 Fördernummer -
1000 Objektart article
1000 Beschrieben durch
1000 @id frl:6405909.rdf
1000 Erstellt am 2017-12-18T16:25:16.151+0100
1000 Erstellt von 218
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1000 Bearbeitet von 218
1000 Zuletzt bearbeitet Fri Dec 04 12:02:51 CET 2020
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1000 Vgl. frl:6405909
1000 Oai Id
  1. oai:frl.publisso.de:frl:6405909 |
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