Intrauterine Growth Retardation Pigs Research Articles

T Cells Development Is Different between Thymus from Normal and Intrauterine Growth Restricted Pig Fetus at Different Gestational Stage.

This experiment was conducted to evaluate the development of T cells in intrauterine growth retarded (IUGR) piglets at different gestational stages, and tentatively explore the relationship between T cells development and the Notch signaling pathway. A total of 18 crossbred (Landrace×Large white) primiparous sows were mated at similar weights and estruses and euthanized at d 60, 90 and 110 of gestation with six replicates for each time point. One IUGR and one normal fetus were picked from each litter. The T-cell subsets, mRNA expression of Delta-like1, Delta-like4, Jagged1, and Notch2 genes in the thymus were investigated. Compared to normal piglets, CD3+CD4−CD8+ cells in IUGR fetuses at d 90 was 0.13% lower (p<0.05). At d 110 of gestation CD8+ T cells in IUGR fetuses was 0.19% lower (p<0.05). The percentage of CD8+ T cells was 3.14% lower (p<0.05) of the total T cells in IUGR pigs at d 60. The abundance of Notch2 and Delta-like4 mRNA at d 110 was 20.93% higher and 0.77% (p<0.05) lower, and Delta-like1 mRNA at d 90 was 0.19% (p<0.05) higher compared to normal pigs. These results suggested that normal fetuses had a greater proportion of T-cell subsets at earlier gestation periods, and the Notch signaling pathway was likely partially responsible for these differences to some degree.

Effects of intrauterine growth retardation and maternal folic acid supplementation on hepatic mitochondrial function and gene expression in piglets

Piglets with intrauterine growth retardation (IUGR) or with normal birth weight (NBW) were selected to evaluate the effects of maternal folic acid supplementation on hepatic mitochondrial function and expression levels of genes involved in mitochondrial DNA (mtDNA) biogenesis and mitochondrial function. During gestation, primiparous Yorkshire sows were fed a Control diet (folic acid 1.3 mg/kg) or a folic acid-supplemented diet (folic acid 30 mg/kg) with 16 replicates per diet. During the 28-d lactation period, sows were fed a common diet. Compared with NBW piglets, hepatic ATP concentrations and mtDNA contents were decreased in IUGR piglets. Furthermore, IUGR piglets exhibited lower membrane potential and decreased oxygen consumption in liver mitochondria, but these parameters were not affected by maternal folic acid supplementation. Intrauterine growth retardation decreased mRNA expression abundance of peroxisomal proliferator-activated receptor-γ coactivator-1α, mitochondrial transcription factor A, uncoupling protein 3, and cytochrome c oxidase subunit I and IV. Impaired antioxidant capacity characterised by increased malondialdehyde content and decreased manganese-superoxide dismutase activity was also observed in IUGR pigs. In IUGR piglets, however, nearly all of these parameters were normalised to the level of NBW piglets when the maternal diet was supplemented with folic acid during pregnancy. Hence, maternal folic acid supplementation was proved to be an effective way to reverse the changes in gene expressions in IUGR pigs, which provided a possible nutritional strategy to improve growth development of IUGR individuals.

Intrauterine growth retardation increases the susceptibility of pigs to high-fat diet-induced mitochondrial dysfunction in skeletal muscle.

It has been recognized that there is a relationship between prenatal growth restriction and the development of metabolic-related diseases in later life, a process involved in mitochondrial dysfunction. In addition, intrauterine growth retardation (IUGR) increases the susceptibility of offspring to high-fat (HF) diet-induced metabolic syndrome. Recent findings suggested that HF feeding decreased mitochondrial oxidative capacity and impaired mitochondrial function in skeletal muscle. Therefore, we hypothesized that the long-term consequences of IUGR on mitochondrial biogenesis and function make the offspring more susceptible to HF diet-induced mitochondrial dysfunction. Normal birth weight (NBW), and IUGR pigs were allotted to control or HF diet in a completely randomized design, individually. After 4 weeks of feeding, growth performance and molecular pathways related to mitochondrial function were determined. The results showed that IUGR decreased growth performance and plasma insulin concentrations. In offspring fed a HF diet, IUGR was associated with enhanced plasma leptin levels, increased concentrations of triglyceride and malondialdehyde (MDA), and reduced glycogen and ATP contents in skeletal muscle. High fat diet-fed IUGR offspring exhibited decreased activities of lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G6PD). These alterations in metabolic traits of IUGR pigs were accompanied by impaired mitochondrial respiration function, reduced mitochondrial DNA (mtDNA) contents, and down-regulated mRNA expression levels of genes responsible for mitochondrial biogenesis and function. In conclusion, our results suggest that IUGR make the offspring more susceptible to HF diet-induced mitochondrial dysfunction.

Effect of folic acid supplementation on hepatic antioxidant function and mitochondrial-related gene expression in weanling intrauterine growth retarded piglets

The aim of the present study was to investigate the effect of dietary folic acid supplementation on antioxidant function and mRNA expression levels of genes involved in mitochondrial biogenesis and function in the liver of piglets affected by intrauterine growth retardation (IUGR). Sixteen piglets at normal birth weight and 16 IUGR piglets were fed either a control diet (C) or a folic acid-supplemented diet (FS, C+5mg/kg folic acid) from 14d of age to 35d of age postnatal. Blood and liver samples were collected at the end of the study. The results showed that body weight was lower for IUGR piglets than that of NBW piglets at 14d of age and 35d of age postnatal (P<0.05). Dietary folic acid supplementation increased plasma folic acid concentrations and hepatic GPx activity, but decreased plasma homocysteine levels (P<0.05). Reduced activities of Mn-SOD and T-AOC, mitochondrial DNA (mtDNA) content, and ATP concentration (P<0.05) were observed in the liver of IUGR pigs fed a control diet. However, the changes in mtDNA content and activities of Mn-SOD and T-AOC were negated in IUGR pigs fed a FS diet (P<0.05). Also, dietary folic acid supplementation decreased protein carbonyls and MDA concentration in the liver of IUGR piglets (P<0.05). Expression levels of genes encoding for PPARγ coactivator-1α (PGC-1α), mammalian silencing information regulator-2α (SIRT-1), nuclear respiratory factor-1 (NRF-1), mt transcription factor A (TFAM), mt single-strand DNA-binding protein (mt SSB), mt polymerase r (mt polr), glucokinase, citrate synthase (CS), ATP synthase (ATPS), and cytochrome c oxidase (CcOX) subunit I and V were decreased in IUGR piglets compared with NBW piglets. However, mRNA levels of PGC-1α, SIRT-1, NRF-1, TFAM, and mt polr in the liver of IUGR pigs fed FS diet were not different from that of NBW pigs. Gene mRNA expression abundance of CcOX IV was enhanced by folic acid supplementation (P<0.05) regardless of birth weight. The present study indicates that IUGR impaired hepatic antioxidant function and mRNA expression levels of genes are involved in mitochondrial biogenesis and function. Dietary folic acid supplementation prevented the harmful effect of IUGR on hepatic antioxidant function and mtDNA biogenesis, but had no effect on mRNA expression levels of genes involved in mitochondrial function.

Effects of Intrauterine Growth Retardation on Development of the Gastrointestinal Tract in Neonatal Pigs

Background: Intrauterine growth retardation (IUGR) is a common problem in human and other species and increases the risk of death of the fetus and newborn during the perinatal period. Objectives: This study was conducted to examine the influences of intrauterine growth retardation (IUGR) on development of the gastrointestinal tract in newborn pigs. Methods: Ten animals from five litters were divided into five piglets with IUGR and five with normal birth-weight (NW). The IUGR category comprised animals with a birth weight 2 SD below the mean birth weight of the total population, while the NW category included animals with a birth weight within one SD of the mean birth weight in the total population. Animals were anesthetized and sampled within 2–4 h after birth and without suckling. The morphological changes of intestine and stomach of IUGR piglets were compared with NW ones. The expressions of IGF-I and receptors for growth hormone and insulin in intestinal mucosa were semiquantified using reverse transcription PCR. Results: The results of our study indicated that the weights of the stomach, small intestine and small intestinal mucosa were significantly lower in IUGR compared with NW piglets (p < 0.01). In addition, the lengths of the small intestine and colon in IUGR pigs were also significantly less than those of NW (p < 0.05). Furthermore, insulin-like growth factor-I (IGF-I) mRNA level in intestinal mucosa of IUGR piglets was increased significantly (p < 0.05), and the expression mRNA levels of insulin receptor and growth hormone (GH) receptor in the mucosa in IUGR piglets showed a tendency to be lower (p = 0.17 and p = 0.11, respectively) than those of the NW animals. Conclusion: We conclude from the data that IUGR affects intestinal growth and morphology and is in associated with altered gene expression of growth-related proteins. We speculate that the morphological change and associated altered endocrine homeostasis contribute to lower growth rates of pigs affected by IUGR.