The digestive function of low birth weight (LBW) pigs post-weaning has been poorly studied. Therefore, newborns from eleven hyperprolific sows were weighed, weaned at 27·2 d and fed a starter diet until sampling. Sampling was done between 18 and 28 d post-weaning. An LBW piglet (n 19) was defined as a piglet having a birth weight less than 1 kg and less than the lower quartile of litter birth weights. Normal birth weight (NBW) piglets (n 13) were having a birth weight close to the mean litter birth weight. For each piglet, eighty-eight variables were determined. Data were analysed with linear models with type of piglet and litter as predictors. A principal component analysis was performed to determine the most important discriminating variables. In the LBW pig, the development of the digestive tract postweaning was delayed: lower small-intestinal weight:length ratio due to a thinner tela submucosa and tunica muscularis and a higher secretory capacity, both in the distal jejunum. These observations might be a consequence of lower circulating insulin-like growth factor-1 (IGF-1) concentrations (126 (SE 10·0) v. 158 (SE 12·0) ng/ml for LBW and NBW, respectively) and a lower density of IGF-1 receptors in the proximal small intestine. Additionally, the plasma antioxidant capacity was lower for the LBW pig. Taken together, in the LBW piglet, the normal gut maturation post-weaning was retarded and this did not seem to be related to the weaning transition as such.

SummarySelection for hyperprolific sows, as a means of increasing litter size and profit, has resulted in an increased number of low-birthweight (LBW) piglets. These LBW piglets might suffer from increased morbidity and mortality during the early neonatal period. In addition, they show reduced growth performance, meat and carcass quality, which leads to an important economic loss for the farmer in the post-natal period. Therefore, nutritional interventions can be undertaken to prevent and rear LBW piglets. In the first part of this review, the preventive strategies at the sow level will be discussed. Approaches in preventing LBW piglets are to optimize the intrauterine environment via supplementing the sow during gestation. In the second part of this review, the interventions at the piglet level will be described. To increase the survival and growth rates of LBW piglets, one must focus on ensuring adequate colostrum and milk intake. Interventions include supplementing piglets, split nursing, split weaning and cross-fostering. Additional interventions increasing the probability of optimal post-natal food intake will be discussed.

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To test the hypothesis that the mucosal maturation of the small intestine is altered in low birth weight piglets, pairs of naturally suckled low birth weight (LBW, n = 20) and normal birth weight (NBW, n = 20) littermate piglets were selected and sampled after 0, 3, 10, and 28 d of suckling. In vivo intestinal permeability was evaluated via a lactulose-mannitol absorption test. Other indirect measurements for mucosal barrier functioning included sampling for histology and immunohistochemistry (intestinal trefoil factor [ITF]), measuring intestinal alkaline phosphatase (IAP) activity, and immunoblotting for occludin, caspase-3, and proliferating cell nuclear antigen (PCNA). The lactulose-mannitol ratio did not differ between NBW and LBW piglets, but a significant increase in this ratio was observed in 28-d-old piglets (P = 0.001). Small intestinal villus height did not differ with age (P = 0.02) or birth weight (P = 0.20). In contrast, villus width (P = 0.02) and crypt depth (P < 0.05) increased gradually with age, but no birth-weight-related differences were observed. LBW piglets had significantly (P = 0.03) more ITF immunoreactive positive cells per villus area compared to NBW piglets, whereas no age (P = 0.82) or region-related (P = 0.13) differences could be observed. The activity of IAP in the small intestine was higher in newborn piglets compared to the older piglets. No significant differences in cell proliferation in the small intestine was observed (P = 0.47) between NBW and LBW piglets; the highest proliferation was seen in piglets of 28 d of age (P = 0.01). Newborn piglets had significantly fewer apoptotic cells, whereas more apoptotic cells were seen in piglets of 10 d of age (P < 0.01). In conclusion, birth weight did not affect the parameters related to intestinal barrier function investigated in this study, suggesting that the mucosal barrier function is not altered in LBW piglets. Nevertheless, these results confirm that the mucosal barrier function in the small intestine of piglets alters with age.

To test the hypothesis that a low molecular weight fraction of colostral whey could affect the morphology and barrier function of the small intestine, 30 3-d-old piglets (normal or low birth weight) were suckled (n = 5), artificially fed with milk formula (n = 5), or artificially fed with milk formula with a low molecular weight fraction of colostral whey (n = 5) until 10 d of age. The small intestine was sampled for histology (haematoxylin and eosin stain; anti-KI67 immunohistochemistry) and enzyme activities (aminopeptidase A, aminopeptidase N, dipeptidylpeptidase IV, lactase, maltase, and sucrase). In addition, intestinal permeability was evaluated via a dual sugar absorption test and via the measurement of occludin abundance. Artificially feeding of piglets reduced final BW (P < 0.001), villus height (P < 0.001), lactase (P < 0.001), and dipeptidylpeptidase IV activities (P < 0.07), whereas crypt depth (P < 0.001) was increased. No difference was observed with regard to the permeability measurements when comparing artificially fed with naturally suckling piglets. Supplementing piglets with the colostral whey fraction did not affect BW, enzyme activities, or the outcome of the dual sugar absorption test. On the contrary, the small intestines of supplemented piglets had even shorter villi (P = 0.001) than unsupplemented piglets and contained more occludin (P = 0.002). In conclusion, at 10 d of age, no differences regarding intestinal morphology and permeability measurements were observed between the 2 BW categories. In both weight categories, the colostral whey fraction affected the morphology of the small intestine but did not improve the growth performances or the in vivo permeability. These findings should be acknowledged when developing formulated milk for neonatal animals with the aim of improving the performance of low birth weight piglets.

Mortality and morbidity of newborn piglets are an economic burden and a threat to animal welfare. Perinatal mortality is particularly high in low birth weight (LBW) piglets. To unravel the possible underlying mechanisms, we investigated the effect of birth weight on morphology of the small intestine, in vivo motility, brush border enzyme activities (lactase, sucrase, maltase, aminopeptidase A, aminopeptidase N and dipeptidylpeptidase IV) and crypt cell proliferation (Ki-67 immunohistochemistry).This was performed in pairs of normal birth weight (NBW; 1.47 ± 0.29 kg) and LBW (0.84 ± 0.21 kg) piglets during the suckling period (0, 3, 10 and 28 d of age). Our study showed no effects on small intestinal morphology, except for an age-related increase in villus width (P = 0.02), crypt depth (P < 0.05) and thickness of the tunica muscularis (P < 0.001). Regarding in vivo small intestinal motility, the peak distribution of the Evans bleu dye (geometric centre) was more progressed in NBW piglets of 28 d of age (P = 0.03) compared to the other groups indicating more propulsive strength. Brush border enzyme activities were similar in NBW and LBW piglets. However, age-and region-related differences were present, except for the aminopeptidase A activity (P = 0.33). Lactase activity was higher in the proximal (P < 0.001) than in the distal part of the small intestine in all age groups and for both regions the lowest in piglets of 28 d old (P < 0.05). In the proximal part of the small intestine, sucrase and maltase activities were increased in 10 and 28 d old piglets (sucrase: P < 0.001; maltase: P < 0.001), whereas in the distal part of the small intestine the highest activities were observed in 28 d old piglets (sucrase: P < 0.005; maltase: P < 0.001). No effect of birth weight (P = 0.74) on the Ki-67 proliferation index was observed. However, 10 d old piglets had less proliferating cells compared to newborn and 28 d old piglets (P = 0.04). Intestinal fatty acid binding protein (i-3 FABP), a marker of damage of the intestinal mucosa was undetectable in LBW and NBW piglets throughout the suckling period. To conclude, birth weight had no influence on small intestinal development and function. However, the results confirm that the development and function of the small intestine alters with age.

Perinatal mortality is high among small-for-gestational age (SGA) piglets and continues to be an economic burden and threat to animal welfare. As the physiological role of serotonin (5-hydroxytryptamine, 5-HT) in perinatal development and gastrointestinal function in the pig remains unknown, the aim of this study was to assess the enteric distribution of 5-HT cells and to determine 5-HT together with its precursor tryptophan in the serum of perinatal normal and SGA piglets. For this purpose, proximal and distal parts of the small intestine (SI) were processed for immunohistochemical analysis to assess the presence of 5-HT endocrine cells. Serum 5-HT was measured with ELISA, whereas its precursor, that is, the free fraction of tryptophan (FFT) together with albumin-bound tryptophan and total tryptophan, were analysed with HPLC in postnatal piglets. In addition, the morphological growth patterns of the different intestinal tissue layers of both normal and SGA piglets were stereologically analysed. The stereological volume density of 5-HT enteroendocrine cells showed a significant interaction effect between age and region. Indeed, the amount of 5-HT cells in both the proximal and distal part of the SI tended to decrease according to age, with the lowest values detected at day 3 postpartum. No differences could be observed related to BW. Interestingly, the serum concentration of 5-HT was higher in normal piglets compared with SGA piglets. Moreover, the ratio of FFT to total tryptophan was significantly affected by age and BW. Normal piglets had, on average, a lower FFT/total tryptophan ratio compared with SGA piglets. An approximate linear decrease was observed with increasing age. Finally, the immaturity of the intestinal system of the SGA piglets was not reflected in altered volume densities of the different intestinal layers. To conclude, although no BW effect could be detected in the distribution of enteric 5-HT cells, serum 5-HT and the ratio of FFT to total tryptophan ratio showed significant differences between normal piglets and their SGA littermates.Keywords: low birth weight, pig, serotonin, serum, small intestine ImplicationsThe use of hyperprolific sows in the pork industry increases the prevalence of prenatal growth-restricted piglets, characterised by reduced survival rates. Serotonin is prominently present in the gastrointestinal system and regulates feeding behaviour and BW. This study investigated the enteric distribution of serotonin cells and the concentration of this hormone along with its precursor tryptophan in the serum of perinatal SGA and normal littermates. These results -combined with the morphological analysis of the small intestine -will give insight into the endocrine programming and morphological adaptations of the small intestine of SGA piglets.

The preterm intestine is immature and responds differently to total parenteral nutrition (TPN) and enteral nutrition, compared with the term intestine. We hypothesised that in preterms, diet composition and feeding route affect mucosal morphology, enterocyte mitosis and apoptosis, and the distribution of laminin-1, fibronectin and collagen IV (extracellular matrix proteins (ECMP)). Preterm piglets (93·5 % of gestation) were delivered via caesarean section and birth weight-matched allocated to one of the four experimental groups: the piglets were either euthanised immediately after delivery, after 3 d of TPN or after 2 d enteral feeding with colostrum or milk formula, following 3 d of TPN. We combined immunohistochemistry, image analysis and stereological measurements to describe the intestinal mucosal layer. No significant changes occurred after 3 d of TPN. Feeding colostrum or milk replacer for 2 d after TPN was associated with an increased crypt depth. Only enteral feeding with colostrum resulted in an increased villus height and mitotic index. Neither TPN nor enteral feeding changed the distribution pattern of ECMP or the occurrence of bifid crypts. The immature distribution pattern of ECMP in TPN-fed piglets, coupled with unchanged enterocyte mitosis and apoptosis indices, illustrates that feeding preterm pigs 3 d TPN does not lead to mucosal atrophy. Despite the invariable distribution of ECMP, colostrum was associated with crypt hyperplasia resulting in an increased villus height. These data illustrate that some mechanisms regulating cell turnover are immature in preterms and may in part explain the abnormal gut responses to TPN and enteral feeding in prematurely born pigs.