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Selenium supplementation inhibits IGF-1 signaling and confers methionine restriction-like healthspan benefits to mice.
- Source :
-
ELife [Elife] 2021 Mar 30; Vol. 10. Date of Electronic Publication: 2021 Mar 30. - Publication Year :
- 2021
-
Abstract
- Methionine restriction (MR) dramatically extends the healthspan of several organisms. Methionine-restricted rodents have less age-related pathology and increased longevity as compared with controls, and recent studies suggest that humans might benefit similarly. Mechanistically, it is likely that the decreased IGF-1 signaling that results from MR underlies the benefits of this regimen. Thus, we hypothesized that interventions that decrease IGF-1 signaling would also produce MR-like healthspan benefits. Selenium supplementation inhibits IGF-1 signaling in rats and has been studied for its putative healthspan benefits. Indeed, we show that feeding mice a diet supplemented with sodium selenite results in an MR-like phenotype, marked by protection against diet-induced obesity, as well as altered plasma levels of IGF-1, FGF-21, adiponectin, and leptin. Selenomethionine supplementation results in a similar, albeit less robust response, and also extends budding yeast lifespan. Our results indicate that selenium supplementation is sufficient to produce MR-like healthspan benefits for yeast and mammals.<br />Competing Interests: JP, SP, JJ No competing interests declared, JT Senior editor, eLife<br /> (© 2021, Plummer et al.)
- Subjects :
- Animal Feed analysis
Animals
Diet
Dietary Supplements analysis
Dose-Response Relationship, Drug
Female
Insulin-Like Growth Factor I metabolism
Male
Mice, Inbred C57BL
Random Allocation
Selenium administration & dosage
Selenomethionine administration & dosage
Sodium Selenite administration & dosage
Insulin-Like Growth Factor I genetics
Methionine administration & dosage
Mice physiology
Selenium metabolism
Selenomethionine metabolism
Sodium Selenite metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 2050-084X
- Volume :
- 10
- Database :
- MEDLINE
- Journal :
- ELife
- Publication Type :
- Academic Journal
- Accession number :
- 33783357
- Full Text :
- https://doi.org/10.7554/eLife.62483