ArticleCommunications biology2026
Glucose enrichment accelerates C. elegans reproductive aging via non-autonomous DAF-2/insulin-like receptor signaling in somatic tissues.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Reproductive systems are highly sensitive to diet, yet the long-term reproductive consequences of overnutrition are poorly defined. Glucose supplementation shortens Caenorhabditis elegans lifespan, and here we find that it also hastens age-related reproductive decline, evidenced by a greater oocyte deterioration and lower fertility with age. 20-mM glucose enrichment still shortens the lifespan of daf-2(e1370) mutants with reduced insulin-like signaling, but unexpectedly, we do not detect detrimental impacts on their reproductive aging phenotypes. Using auxin-induced tissue-selective degradation, we show that DAF-2/insulin-like receptor signaling in C. elegans intestine and body wall musculature is required for glucose enrichment to impair reproductive function of aged worms, and DAF-2 degradation in either tissue protects against glucose-induced reproductive aging. We also observe that disrupting lipid homeostasis via RNAi against the lipl-4 lipase can impair daf-2(e1370) reproductive function under glucose enrichment. Therefore, insulin-like signaling in metabolically active somatic tissues could represent a key link between overnutrition and reproductive aging.
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