Glucose enrichment accelerates C. elegans reproductive aging via non-autonomous DAF-2/insulin-like receptor signaling in somatic tissues

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dc.contributor.authorAthar, Faria
dc.contributor.authorHouston, Emma J.
dc.contributor.authorJewett, Emily
dc.contributor.authorTempleman, Nicole M.
dc.date.accessioned2026-05-07T17:31:18Z
dc.date.available2026-05-07T17:31:18Z
dc.date.issued2025
dc.description.abstractDetrimental effects of chronic high-sugar overconsumption can extend from molecular and cellular responses to systemic changes. Reproductive systems are particularly sensitive to diet and energetic state, yet the long-term reproductive consequences of overnutrition are poorly defined. Here, we used Caenorhabditis elegans to study the impacts of glucose excess on reproductive aging. Glucose supplementation shortens C. elegans lifespan, and we found that it also hastens age-related reproductive decline, evidenced by a greater deterioration in oocyte quality and lower fertility with age. We next evaluated insulin-like signaling contributions, as this glucose-responsive pathway is well known to regulate both somatic aging and reproductive aging. Intriguingly, while 20 mM glucose enrichment still shortens the lifespan of daf-2(e1370) mutants, we found that it had no detrimental impact on their reproductive aging phenotypes. Using auxin-induced tissue-selective degradation, we discovered that DAF-2/insulin-like receptor signaling in C. elegans intestine and body wall musculature is required for glucose enrichment to exert damaging impacts on the reproductive system. However, suppressing insulin-like signaling in either of these tissues is sufficient to protect C. elegans against glucose-induced reproductive aging. These findings suggest that insulin-like signalling in metabolically active somatic tissues may represent a key link between overnutrition and reproductive aging.
dc.description.reviewstatusReviewed
dc.description.scholarlevelFaculty
dc.description.sponsorshipThis study was supported by funding from the Natural Sciences Engineering Research Council of Canada (RGPIN-2022-05149). Worm strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). N.M.T. is a Tier 2 Canada Research Chair in Cell Biology, a Michael Smith Health Research BC Scholar, and a member of the Sexual and Reproductive Health and Rights Research Cluster at the University of Victoria.
dc.identifier.citationAthar, F., Houston, E. J., Jewett, E., & Templeman, N. M. (2025). Glucose enrichment accelerates C. elegans reproductive aging via non-autonomous DAF-2/insulin-like receptor signaling in somatic tissues. bioRxiv. https://doi.org/10.1101/2025.07.04.663088
dc.identifier.urihttps://doi.org/10.1101/2025.07.04.663088
dc.identifier.urihttps://hdl.handle.net/1828/23844
dc.language.isoen
dc.publisherbioRxiv
dc.rightsCC BY-NC-ND
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectSexual and Reproductive Health and Rights (SRHR) Aspiration Research Cluster
dc.subject.departmentDepartment of Biology
dc.titleGlucose enrichment accelerates C. elegans reproductive aging via non-autonomous DAF-2/insulin-like receptor signaling in somatic tissues
dc.typePreprint

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