Endoplasmic Reticulum Stress Contributes to Intestinal Injury in Intrauterine Growth Restriction Newborn Piglets.

Area of Science:

• Veterinary Medicine
• Developmental Biology
• Gastroenterology

Background:

• Intrauterine growth retardation (IUGR) in piglets causes high neonatal morbidity and mortality.
• Gut dysfunction is a primary contributor to post-birth complications in IUGR piglets.
• Mechanisms underlying IUGR-related gut dysfunction are not fully understood.

Purpose of the Study:

• To investigate the effects of IUGR on intestinal structure, digestive function, endoplasmic reticulum stress (ERS), apoptosis, barrier function, and inflammation in newborn piglets.
• To elucidate the molecular pathways involved in IUGR-induced gut dysfunction.

Main Methods:

• Comparative study of IUGR and normal birth weight piglets.
• Analysis of jejunal morphology and villus height.
• Measurement of serum glucose and lactase levels.
• Assessment of mRNA and protein expression related to ERS, apoptosis, barrier function, and inflammation.

Main Results:

• IUGR piglets exhibited reduced jejunal villi height and villus-to-crypt ratio.
• IUGR piglets showed shorter microvilli, mitochondrial swelling, and endoplasmic reticulum expansion.
• IUGR led to decreased serum glucose and lactase, but increased jejunal mRNA levels of ERS, apoptosis, barrier, and inflammatory markers.
• Elevated GRP78 protein levels were observed in IUGR piglets.

Conclusions:

• IUGR significantly impairs intestinal structure and barrier function in newborn piglets.
• IUGR activates endoplasmic reticulum stress (ERS) and inflammatory responses in the jejunum.
• ERS-related apoptosis pathways are activated, contributing to gut dysfunction and potentially mortality in IUGR piglets.