Selenium supplementation inhibits IGF-1 signaling and confers methionine restriction-like healthspan benefits to mice.

TitleSelenium supplementation inhibits IGF-1 signaling and confers methionine restriction-like healthspan benefits to mice.
Publication TypeJournal Article
Year of Publication2021
AuthorsPlummer JD, Postnikoff SDl, Tyler JK, Johnson JE
JournalElife
Volume10
Date Published2021 03 30
ISSN2050-084X
KeywordsAnimal Feed, Animals, Diet, Dietary Supplements, Dose-Response Relationship, Drug, Female, Insulin-Like Growth Factor I, Male, Methionine, Mice, Mice, Inbred C57BL, Random Allocation, Selenium, Selenomethionine, Sodium Selenite
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.

DOI10.7554/eLife.62483
Alternate JournalElife
PubMed ID33783357
PubMed Central IDPMC8009673
Grant ListR01 AG050660 / AG / NIA NIH HHS / United States
CCL023-CCL025 / / Orentreich Foundation for the Advancement of Science /
R01 AG050660 / NH / NIH HHS / United States
Related Faculty: 
Jessica K. Tyler, Ph.D.

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