Capsaicin diet drives gut inflammation and exosomal miR-17-3p elevation in idiopathic short stature

Nat Commun. 2025 Dec 30;17(1):1123. doi: 10.1038/s41467-025-67883-2.

Abstract

Idiopathic short stature (ISS) remains a major pediatric challenge with unclear causes and inconsistent responses to growth hormone therapy. Here we show that plasma exosomes from children with ISS contain elevated hsa-miR-17-3p that disrupts growth signaling and impairs cartilage cell proliferation. Elevated miR-17-3p suppresses ZNF148/SOS1 signaling, linking molecular dysfunction to dietary exposure in ISS. To investigate environmental triggers, we developed a capsaicin-rich diet rat model that recapitulates ISS, showing normal Gh/Igf-1 levels but elevated plasma miR-17-3p. The diet induced mild gut inflammation, increasing miR-17-3p in intestinal and plasma exosomes. Fecal samples from ISS children exhibited similar elevations in miR-17-3p and inflammatory markers, linking spicy diets to ISS pathogenesis. Finally, engineered exosomes designed to silence miR-17-3p, combined with localized growth hormone therapy, restored growth plate function. These findings uncover a diet-driven exosome axis underlying ISS and suggest new therapeutic strategies for children in high-capsaicin regions.

MeSH terms

  • Animals
  • Capsaicin* / adverse effects
  • Cell Proliferation
  • Child
  • Child, Preschool
  • Diet* / adverse effects
  • Disease Models, Animal
  • Exosomes* / genetics
  • Exosomes* / metabolism
  • Female
  • Growth Disorders* / genetics
  • Growth Disorders* / metabolism
  • Humans
  • Inflammation / chemically induced
  • Insulin-Like Growth Factor I / metabolism
  • Male
  • MicroRNAs* / blood
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction

Substances

  • MicroRNAs
  • MIRN17 microRNA, human
  • Capsaicin
  • Insulin-Like Growth Factor I