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Prenatal caffeine exposure in rats causes fetal liver dysfunction and intrauterine growth retardation. This programming involves altered glucocorticoid and IGF1 signaling, impacting liver development and stress response in offspring.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Hepatology

Background:

  • Prenatal caffeine exposure (PCE) is linked to intrauterine growth retardation (IUGR) and nonalcoholic fatty liver disease susceptibility in offspring.
  • Maternal glucocorticoid overexposure is implicated as a mechanism underlying PCE-induced IUGR and subsequent liver disease.

Purpose of the Study:

  • To investigate the impact of PCE on fetal liver development and identify its programming mechanisms.
  • To explore the role of the glucocorticoid-IGF1 axis in mediating PCE's effects on liver development.

Main Methods:

  • In vivo studies using rat models exposed to PCE during gestation.
  • Analysis of fetal and offspring serum hormone levels (corticosterone, IGF1).
  • Gene expression analysis of glucocorticoid (GR/C/EBPα) and IGF1 signaling (IGF1/IGF1R/Akt2) pathways in liver tissues.
  • In vitro experiments using cortisol to mimic glucocorticoid effects.

Main Results:

  • PCE resulted in reduced fetal weight, increased IUGR, and fetal liver developmental dysfunction.
  • Elevated fetal corticosterone and suppressed IGF1 were observed, alongside altered GR/C/EBPα and IGF1 signaling pathways.
  • Offspring exhibited catch-up growth and improved liver function by postnatal day 6, but adult offspring showed altered stress responses.
  • In vitro, cortisol upregulated GR/C/EBPα and downregulated IGF1R, suggesting a direct role of glucocorticoids.

Conclusions:

  • PCE induces fetal liver developmental dysfunction and IUGR in rats through intrauterine programming.
  • The mechanism involves the dysregulation of the liver's glucocorticoid-IGF1 axis, characterized by increased GR/C/EBPα and decreased IGF1/IGF1R signaling.
  • These prenatal programming effects influence liver function and stress responses throughout development.