TitleDietary resveratrol increases mid-life fecundity of female Nothobranchius guentheri.
Publication TypeJournal Article
Year of Publication2018
AuthorsLee Y, Drake AC, Thomas NO, Ferguson LG, Chappell PE, Shay KPetersen
JournalComp Biochem Physiol C Toxicol Pharmacol
Volume208
Pagination71-76
Date Published2018 Jun
ISSN1532-0456
KeywordsAge Factors, Animal Feed, Animals, Antioxidants, Body Weight, Diet, Female, Fertility, Fish Proteins, Fishes, Nicotinamide Phosphoribosyltransferase, Ovary, Resveratrol, Sexual Maturation, Sirtuin 1, Stilbenes
Abstract

The decline of female reproductive function is an early phenotype of aging in humans, occurring only midway through the lifespan. Yet the number of women delaying pregnancy continues to rise in industrialized societies due to personal or socioeconomic circumstances, often resulting in subfertility or difficulty conceiving. There are few defined mechanisms associated with this etiology, and equally few effective therapies. To combat this problem, we used a novel emerging model, Nothobranchius guentheri, that recapitulates the age-associated spectrum of changes that adversely affect human fertility. We hypothesized that resveratrol (RSV), which activates SirT1 as an oxidative stress sensor and longevity assurance enzyme, would improve female fecundity in mid-life. RSV, a polyphenol found in grapes and red wine, has been touted as an anti-aging dietary supplement due to its ability to prolong both lifespan and health span. SirT1 is an NAD+ dependent histone deacetylase, whose activity is regulated by the nicotinamide to NAD+ salvage pathway, especially the rate-limiting enzyme NAMPT. We found that female N. guentheri fed 600μgRSV/g food into mid-life (~20weeks), beginning at sexual maturity, showed increased embryo production compared to those on Control diet. Furthermore, the RSV-fed fish had significantly increased NAMPT. This suggests that dietary RSV has a positive effect on female fertility, and that it may become an effective therapy to regulate sirtuin activity and combat reproductive senescence.

DOI10.1016/j.cbpc.2017.10.006
Alternate JournalComp. Biochem. Physiol. C Toxicol. Pharmacol.
PubMed ID29054583
PubMed Central IDPMC5906208
Grant ListT32 AT002688 / AT / NCCIH NIH HHS / United States