Glucose substitution prolongs maintenance of energy homeostasis and lifespan of telomere dysfunctional mice.
Nat Commun
; 5: 4924, 2014 Sep 18.
Article
em En
| MEDLINE
| ID: mdl-25233189
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.
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1
Base de dados:
MEDLINE
Assunto principal:
Telômero
/
Glucose
Limite:
Animals
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article