Abstract

The intestine of intrauterine growth retarded (IUGR) neonates showed different morphology compared to neonates born with normal body weight (NBW). The aim of the present study was to investigate the ultrastructure and proteomic profile of the gut epithelium in IUGR pig neonates with special attention to the digestive and absorptive function. Intestine tissue samples were investigated in 7-day-old IUGR and NBW littermate piglets using histometry, immunofluorescence, scanning electron microscopy (SEM), and mass spectrometry analysis. IUGR piglets have shown reduced mucosa and muscularis thickness and an enhanced number of foetal type enterocytes (FTE). SEM studies have shown the lack of the characteristic large-size vacuole in IUGR's enterocytes. Delayed removal of FTE in IUGR neonates was probably due to the inhibited apoptosis in the apical part of villi and increased apoptosis and reduced mitosis in the crypt region. In the expression of proteins in the intestinal mucosa such as hexokinase I, histones, and prelamin A/C, carbamoyl phosphate was reduced in IUGR neonates. Finally, IUGR intestines showed higher expression of HSPA9 and HSPA5 as apoptosis markers. The data indicate modifications of gut mucosa in IUGRs that may result in slower gut mucosa maturation and reduced utilisation of nutrient as compared to NBW pig neonates.

Highlights

  • Intrauterine growth retarded (IUGR) newborn piglet is born on time, and it is characterised by low birth body mass, high perinatal mortality, and a “dolphin-like” head shape compared with “normal” piglets [1, 2]

  • The asymmetric IUGR syndrome was confirmed in pig neonates by low birth body weight, head shape, brain weight (Table 1), and clinical examination at birth

  • At postnatal day 7 (PD7), the body weight, liver weight, and small intestine weight and size were significantly lower in IUGR piglets as compared to their normal body weight (NBW) littermates (Table 1)

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Summary

Introduction

Intrauterine growth retarded (IUGR) newborn piglet is born on time, and it is characterised by low birth body mass (below 1.1 kg), high perinatal mortality, and a “dolphin-like” head shape compared with “normal” piglets [1, 2]. In IUGRs, a catch-up-growth (CAG) is observed, which is the time when neonates are able to compensate their low body birth weight by accumulation of adipose tissue in visceral area, rather than by muscle mass growth. Proteomic studies by Wang et al [7] revealed that cellular signalling defects, redox imbalance, reduced protein synthesis, and enhanced proteolysis could be Disease Markers major mechanisms responsible for abnormal absorption and metabolism of nutrients, as well as reduced growth and impaired development of the small intestine, liver, and muscle in IUGR neonates. The more recent paper by Wang et al [8] indicates that small intestinal mucosal permeability and mRNA expression of redox-sensitive genes is affected in IUGR piglets

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