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<p>Reproductive systems are highly sensitive to diet, yet the long-term reproductive consequences of overnutrition are poorly defined. Glucose supplementation shortens <i>Caenorhabditis elegans</i> 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 <i>daf-2(e1370)</i> 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 <i>C. elegans</i> 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 <i>lipl-4</i> lipase can impair <i>daf-2(e1370)</i> reproductive function under glucose enrichment. Therefore, insulin-like signaling in metabolically active somatic tissues could represent a key link between overnutrition and reproductive aging.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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  • Faria Athar,
  • Emma J. Houston,
  • Emily Jewett,
  • Chelsey K. May,
  • Manuel Centeno Duque,
  • Nicole M. Templeman

摘要

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.