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El azúcar parece prolongar la vida en la vejez

El azúcar parece prolongar la vida en la vejez



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El azúcar parece prolongar la vida en la vejez

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  • 25/09/14
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En general, se considera que la reducción de la cantidad de calorías y de azúcar son medidas adecuadas para la prevención de las enfermedades y la prolongación de la vida. De acuerdo con un estudio alemán, esto únicamente parece cumplirse en los jóvenes y adultos de mediana edad y, de hecho, es posible que ocurra lo contrario en la vejez. De acuerdo con «Nature Communications», los médicos hallaron que un aumento de la ingesta de glucosa prolongaba la esperanza de vida de los animales en algunos modelos en ratones.
Se sabe que la esperanza de vida se correlaciona con la longitud de los telómeros. En su estudio sobre ratones, los científicos del Leibniz Institut für Altersforschungt - Fritz Lipmann-Institut e.V. (FLI) (Jena, Alemana) demostraron que, con la edad, el acortamiento de los telómeros aumenta la demanda de energía de las células y los tejidos, con lo que también se aumenta la demanda de glucosa.
Los investigadores descubrieron que los ratones de más edad con telómeros cortos que recibían una alimentación rica en glucosa mostraban un 20 por ciento de aumento de la esperanza de vida global. Según explicó el coautor Bernhard Boehm, de la Universität Ulm: «Estos resultados resultaron muy sorprendentes y pueden proporcionar una explicación del cambio en la correlación del peso corporal y la esperanza de vida en los mayores en comparación con las personas de mediana edad». De hecho, el aumento del peso corporal en las personas de mediana edad se relaciona con una menor esperanza de vida y un aumento del riesgo de aparición de enfermedades mientras que, en los años posteriores, esta relación es precisamente la contraria.
El autor principal de la publicación, Lenhard Rudolph, indica: «Ahora debe comprobarse si los resultados de nuestro estudio también se cumplen en los seres humanos. En ese caso, es posible que tengamos que cambiar la composición de nuestra alimentación en las edades avanzadas para mantener el funcionamiento de nuestros tejidos y células, los cuales muestran un aumento de la demanda de restitución de glucosa para la producción de energía». Ya se han puesto en marcha los primeros estudios piloto.

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

Nature Communications
 
5,
 
Article number:
 
4924
 
doi:10.1038/ncomms5924
Received
 
Accepted
 
Published
 

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 ​glucosethus 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 ​glucosesubstitution for the maintenance of energy homeostasis and ​IGF-1/​mTOR-dependent mitochondrial biogenesis in ageing tissues.
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  1. Glucose feeding extends lifespan of telomere dysfunctional mice.
    Figure 1
  2. Glucose supplementation rescues thymus atrophy and IGF-1 and glucose levels of telomere dysfunctional mice.
    Figure 2
  3. Telomere dysfunctional mice show elevated glucose depletion rates and glucose supplementation rescues catabolic metabolism in this context.
    Figure 3
  4. Glucose supplementation improves energy homeostasis of telomere dysfunctional mice by increasing glycolysis and oxidative glucose metabolism.
    Figure 4
  5. Glucose supplementation rescues mitochondrial mass and increases oxygen consumption and ATP levels in G3 mTerc−/− mice.
    Figure 5
  6. DNA damage signalling impairs mitochondrial biogenesis and function in ageing G3 mTerc−/− mice.
    Figure 6
  7. Suppression of IGF-1 and mTOR contributes to impairments in mitochondrial biogenesis and function in ageing G3 mTerc−/− mice.
    Figure 7
  8. Model of telomere dysfunction-induced metabolic changes that accelerate tissue ageing.
    Figure 8
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Author information

  1. These authors contributed equally to this work.

    • Pavlos Missios, 
    • Yuan Zhou, 
    • Luis Miguel Guachalla & 
    • Guido von Figura

  2. Present address: Director of Metabolic Medicine NTU Singapore and Imperial College London.

    • Bernhard O. Böhm

Affiliations

  1. Cooperation Group of the Leibniz Institute for Age Research—Fritz-Lipmann-Institute (FLI) Jena with the University of Ulm, 89081 Ulm, Germany

    • Pavlos Missios,
      •  
    • Yuan Zhou,
      •  
    • Luis Miguel Guachalla,
      •  
    • Guido von Figura,
      •  
    • Sundaram Reddy Chakkarappan &
      •  
    • Zhangfa Song

  2. Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 7, avenue des Hauts-Fourneaux, Esch-Belval L-4362, Luxembourg

    • Andre Wegner,
      •  
    • Tina Binz &
      •  
    • Karsten Hiller

  3. Leibniz Institute for Age Research—Fritz Lipmann Institute (FLI), Beutenbergstr 11, 07745 Jena, Germany

    • Anne Gompf,
      •  
    • Götz Hartleben,
      •  
    • Martin D. Burkhalter,
      •  
    • Cagatay Günes &
      •  
    • K. Lenhard Rudolph

  4. Institute for Genetics, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Street 47A, 50674 Cologne, Germany

    • Veronika Wulff &
      •  
    • Tina Wenz

  5. Institute of Epidemiology, Ingolstädter Landstrasse 1, 85764 Munich/Neuherberg, Germany

    • Rui Wang Sattler &
      •  
    • Thomas Illig

  6. German Institute of Human Nutrition, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany

    • Susanne Klaus

  7. Department of Internal Medicine I, University of Ulm, 89081 Ulm, Germany

    • Bernhard O. Böhm

Contributions

P.M., Y.Z., L.M.G. and G.v.F. contributed to equal parts. P.M., Y.Z., L.M.G. and G.v.F. performed most of the experiments, were involved together with K.L.R. in design and analysis of the experiments, as well as in preparation of the manuscript. A.W., T.B. and K.H. performed ​glucosetracing experiments. S.R.C. was involved in the ​IGF-1 injection experiment. A.G. was involved in the survival experiments. G.H., M.D.B. and C.G. performed Seahorse experiments. V.W. and T.W. did investigations on mitochondria. R.W.S. and T.I. performed the metabolomics experiments. Z.S. was involved in thymus experiments. S.K. did bomb calorimetry and stool analysis. B.O.B. was involved in ​IGF-1 experiments as well as preparation of the manuscript. K.L.R. conceived the study.

Competing financial interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to: 

Supplementary information

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    Supplementary Figures 1-5 and Supplementary Tables 1-2

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