SIRT1 Gain of Function Does Not Mimic or Enhance the Adaptations to Intermittent Fasting.
- Boutant M Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland.
- Kulkarni SS Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland.
- Joffraud M Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland.
- Raymond F Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland.
- Métairon S Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland.
- Descombes P Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland; École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
- Cantó C Nestlé Institute of Health Sciences (NIHS), 1015 Lausanne, Switzerland; École Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland. Electronic address: carlos.cantoalvarez@rd.nestle.com.
- 2016-03-01
Published in:
- Cell reports. - 2016
SIRT1
caloric restriction
mitochondria
Adaptation, Physiological
Animals
Fasting
Gene Expression
Glucose
Insulin Resistance
Liver
Male
Mice, Transgenic
Muscle, Skeletal
Physical Conditioning, Animal
Sirtuin 1
Transcriptome
English
Caloric restriction (CR) has been shown to prevent the onset of insulin resistance and to delay age-related physiological decline in mammalian organisms. SIRT1, a NAD(+)-dependent deacetylase enzyme, has been suggested to mediate the adaptive responses to CR, leading to the speculation that SIRT1 activation could be therapeutically used as a CR-mimetic strategy. Here, we used a mouse model of moderate SIRT1 overexpression to test whether SIRT1 gain of function could mimic or boost the metabolic benefits induced by every-other-day feeding (EODF). Our results indicate that SIRT1 transgenesis does not affect the ability of EODF to decrease adiposity and improve insulin sensitivity. Transcriptomic analyses revealed that SIRT1 transgenesis and EODF promote very distinct adaptations in individual tissues, some of which can be even be metabolically opposite, as in brown adipose tissue. Therefore, whereas SIRT1 overexpression and CR both improve glucose metabolism and insulin sensitivity, the etiologies of these benefits are largely different.
- Language
-
- English
- Open access status
- gold
- Identifiers
-
- DOI 10.1016/j.celrep.2016.02.007
- PMID 26923584
- Persistent URL
- https://sonar.ch/global/documents/204229
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