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Missios, P.* ; Zhou, Y.* ; Guachalla, L.M.* ; von Figura, G.* ; Wegner, A.* ; Chakkarappan, S.R.* ; Binz, T.* ; Gompf, A.* ; Hartleben, G.* ; Burkhalter, M.D.* ; Wulff, V.* ; Günes, C.* ; Wang-Sattler, R. ; Song, Z.* ; Illig, T. ; Klaus, S.* ; Böhm, B.O.* ; Wenz, T.* ; Hiller, K.* ; Rudolph, K.L.*

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

Nat. Commun. 5:4924 (2014)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 5, Heft: , Seiten: , Artikelnummer: 4924 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed