Intestinal Development in Intrauterine Growth-Restricted Piglets

Intrauterine growth restriction (IUGR) in piglets impairs the normal maturation of the small and large intestine, leading to reduced nutrient absorption, compromised barrier integrity and heightened susceptibility to inflammation. A hallmark of IUGR is a lower villus height to crypt depth ratio, reflecting a diminished absorptive surface and altered epithelial renewal. Brush-border enzyme activities such as lactase and maltase are often suppressed, further limiting carbohydrate digestion. At the cellular level, IUGR piglets exhibit increased oxidative damage, elevated enterocyte apoptosis and weakened tight junctions, which together undermine mucosal defence. Immune responses in the gut are skewed towards a pro-inflammatory profile, with alterations in cytokine production that can exacerbate barrier dysfunction. Concurrently, the establishment of the intestinal microbiota is disrupted, with decreases in beneficial short-chain fatty acid (SCFA)–producing taxa and expansion of opportunistic or pro-inflammatory groups. These changes persist beyond the neonatal period and can influence long-term growth, feed efficiency and resistance to enteric disease. Understanding the interplay between morphological, biochemical and microbial factors in IUGR provides a foundation for nutritional or pharmaceutical interventions aimed at restoring intestinal health in affected piglets.

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Intestinal Development in Intrauterine Growth-Restricted Piglets publication trend

The graph below shows the total number of articles in intestinal development in intrauterine growth-restricted piglets across all publications each year (not limited to Nature Index journals).

Technical terms

Intrauterine growth restriction (IUGR): Impaired fetal growth in utero resulting in low birth weight and organ immaturity.

Villus height to crypt depth ratio: A measure of intestinal mucosal architecture; lower ratios indicate reduced absorptive capacity.

Dysbiosis: An imbalance in the composition or function of the gut microbiota, often linked to disease.

Short-chain fatty acids (SCFAs): Fermentation products of dietary fibres by gut microbes that support epithelial health and immune regulation.

Bile acids: Steroid acids synthesised in the liver that emulsify dietary fats and act as signalling molecules in the gut.

M2 macrophage polarization: A functional state of macrophages characterised by anti-inflammatory and tissue-repair activities.

Nrf2/Keap1 pathway: A cellular antioxidant defence mechanism in which Nrf2 drives expression of detoxifying enzymes when released from Keap1 inhibition.

TLR4-NF-κB/ERK pathway: An innate immune signalling cascade activated by microbial or stress signals, leading to pro-inflammatory gene expression.

References

1. Gut microbiota-derived ursodeoxycholic acid alleviates low birth weight-induced colonic inflammation by enhancing M2 macrophage polarization. Microbiome (2023).
2. Intrauterine Growth Restriction Affects Colonic Barrier Function via Regulating the Nrf2/Keap1 and TLR4-NF-κB/ERK Pathways and Altering Colonic Microbiome and Metabolome Homeostasis in Growing–Finishing Pigs. Antioxidants (2024).
3. Dietary bile acid supplementation in weaned piglets with intrauterine growth retardation improves colonic microbiota, metabolic activity, and epithelial function. Journal of Animal Science and Biotechnology (2023).