The Impact of Prenatal Exposure to Dexamethasone on Gastrointestinal Function in Rats

PLoS One. 2016 Sep 1;11(9):e0161750. doi: 10.1371/journal.pone.0161750. eCollection 2016.

Abstract

Antenatal treatment with synthetic glucocorticoids is commonly used in pregnant women at risk of preterm delivery to accelerate tissue maturation. Exposure to glucocorticoids during development has been hypothesized to underlie different functional gastrointestinal (GI) and motility disorders. Herein, we investigated the impact of in utero exposure to synthetic glucocorticoids (iuGC) on GI function of adult rats. Wistar male rats, born from pregnant dams treated with dexamethasone (DEX), were studied at different ages. Length, histologic analysis, proliferation and apoptosis assays, GI transit, permeability and serotonin (5-HT) content of GI tract were measured. iuGC treatment decreased small intestine size and decreased gut transit. However, iuGC had no impact on intestinal permeability. iuGC differentially impacts the structure and function of the GI tract, which leads to long-lasting alterations in the small intestine that may predispose subjects prone to disorders of the GI tract.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Proliferation / drug effects
  • Dexamethasone / adverse effects*
  • Female
  • Gastrointestinal Motility / drug effects
  • Intestine, Small / drug effects*
  • Intestine, Small / metabolism
  • Intestine, Small / pathology
  • Intestine, Small / physiopathology*
  • Male
  • Organ Size / drug effects
  • Permeability / drug effects
  • Pregnancy
  • Prenatal Exposure Delayed Effects / metabolism
  • Prenatal Exposure Delayed Effects / pathology
  • Prenatal Exposure Delayed Effects / physiopathology*
  • Rats
  • Rats, Wistar
  • Serotonin / metabolism

Substances

  • Serotonin
  • Dexamethasone

Grants and funding

We acknowledge the Portuguese Foundation for Science and Technology (FCT) for providing a fellowship to Fátima Ramalhosa (SFRH/BD/52058/2012) and Carina Soares-Cunha (SFRH/BD/51992/2012).