Glucose substitution prolongs maintenance of energy homeostasis and lifespan of telomere dysfunctional mice

Pavlos Missios, Yuan Zhou, Luis Miguel Guachalla, Guido von Figura, Andre Wegner, Sundaram Reddy Chakkarappan, Tina Binz, Anne Gompf, Götz Hartleben, Martin D. Burkhalter, Veronika Wulff, Cagatay Günes, Rui Wang Sattler, Zhangfa Song, Thomas Illig, Susanne Klaus, Bernhard O. Böhm, Tina Wenz, Karsten Hiller and K. Lenhard Rudolph ()
Additional contact information
Pavlos Missios: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Yuan Zhou: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Luis Miguel Guachalla: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Guido von Figura: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Andre Wegner: Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 7, avenue des Hauts-Fourneaux
Sundaram Reddy Chakkarappan: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Tina Binz: Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 7, avenue des Hauts-Fourneaux
Anne Gompf: Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11
Götz Hartleben: Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11
Martin D. Burkhalter: Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11
Veronika Wulff: Institute for Genetics, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Street 47A
Cagatay Günes: Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11
Rui Wang Sattler: Institute of Epidemiology, Ingolstädter Landstrasse 1
Zhangfa Song: Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm
Thomas Illig: Institute of Epidemiology, Ingolstädter Landstrasse 1
Susanne Klaus: German Institute of Human Nutrition, Arthur-Scheunert-Allee 114-116
Bernhard O. Böhm: University of Ulm
Tina Wenz: Institute for Genetics, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Street 47A
Karsten Hiller: Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 7, avenue des Hauts-Fourneaux
K. Lenhard Rudolph: Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract 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.

Date: 2014
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DOI: 10.1038/ncomms5924

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