Growth Of Gastrointestinal Tract Research Articles

Invited review: Aspects of gastrointestinal tract growth and maturation in the pre- and postweaning period of pigs

The growth and development of the gastrointestinal tract (GIT) of the young pig, both before and after parturition, is critical for the ani-mal’s future growth and development, efficiency of feed conversion to body depots, and, ultimately, its survival. The perinatal development of the GIT encompasses a prenatal phase, a neonatal phase, and the postweaning phase, which is associated with the adaptation of the GIT to utilize solid feed after the piglet is weaned. The consumption of colostrum, initially, and then milk after birth provides nutrients and compounds for piglets that are critically important as stimuli and substrates to the GIT that in turn evoke a suite of anatomical, immunological, biochemical, physiological, and regulatory processes that advance the overall maturity of the GIT. However, at weaning the combined influence of the various stressors imposed causes a hiatus in the growth and development of the GIT, such that the newly weaned pig endures a “growth check” while exposing it to a greater disease and health risk. Low and variable feed intake is a major outcome of the weaning process, but nevertheless, there are numerous nutritional/manage-ment interventions producers can implement in an attempt to overcome this major issue. This review summarizes some major aspects of, and influences on, GIT growth, development, and maturation in the pre- and postweaning period of pigs, demonstrating that postnatal influences occur in utero and that evolution of the GIT continues to occur after weaning.

Prenatal development of gastrointestinal function in the pig and the effects of fetal esophageal obstruction.

Maturation of the fetal gastrointestinal tract (GIT) is influenced by both luminal stimuli (e.g. swallowed fluid) and hormonal factors (e.g. endogenous cortisol release). The aims of the present study were 1) to investigate GIT growth and maturation during the last 20% of gestation in pigs (term = 114 +/- 2 d), and 2) to investigate the effect of esophageal ligation, to prevent fetal swallowing, at 80% to 91% gestation. In normal fetuses, marked increases occurred during late gestation in body weight (+95%), relative intestinal weight (+79%, g kg(-1) body weight), activity of some digestive enzymes (1.5- to 10-fold), and absorption of glucose and intact proteins (3- to 6-fold). Fetuses with ligated esophagi had lowered body weight (-20%), reduced intestinal weight (-43%), aminopeptidase A activity (-24%), and glucose absorption (-27%), while lactase, sucrase, and dipeptidylpeptidase IV activities were increased (+40-50%), compared with sham-operated fetuses (all p < 0.05). Other parameters of GIT function remained unchanged by esophageal obstruction (absorption of amino acids and immunoglobulin, activity of chymosin, amylase, trypsin, chymotrypsin, maltase, aminopeptidase N -- all expressed per gram GIT tissue). Ligated fetuses had elevated cortisol levels, which is known to stimulate fetal GIT maturation. We conclude that the rapid development of GIT function in late gestation is diminished by esophageal obstruction, mainly due to slower GIT growth and not inhibition of normal functional development of enterocytes.

How does the foetal gastrointestinal tract develop in preparation for enteral nutrition after birth?

At birth, the gastrointestinal tract (GIT) must be able to cope with the shift from parenteral nutrition before birth (via the placenta) to enteral nutrition after birth (oral colostrum/milk intake). In preparation for this event, the GIT grows and matures very rapidly in the weeks before birth. A series of studies in foetal pigs and sheep have shown that both hormonal and luminal factors influence this rapid phase of GIT development in farm animals. Among the potential hormonal regulators of development, cortisol plays a pivotal role. Thus, the normal developmental increases in stomach acid and gastrin secretion, and in certain enzyme activities (chymosin, pepsin, amylase, lactase, aminopeptidases), are stimulated by circulating cortisol. Cortisol also affects the intestinal absorption of immunoglobulins at birth but has limited effects on the GIT in the postnatal period. Ingestion of amniotic fluid by the foetus and of colostrum by the neonate also modulates GIT growth and enzyme activities. These effects may be mediated via luminal actions of growth factors, hormones and nutrients present in the fluids. However, luminal influences on the developing GIT are less pronounced in the foetus than in the neonate. In conclusion, both circulating and luminal factors affect prenatal GIT development to ensure that the foetal GIT is sufficiently mature to support the dramatic changes in nutrition that occur at birth.

Restriction of Nutrition In Utero Selectively Inhibits Gastrointestinal Growth in Fetal Sheep , ,

This study examined the effects of reduced nutrition on fetal growth over the first half of gestation. Reduced nutrition was achieved by a combination of reduced maternal food intake and carunclectomy, a procedure which restricts the development of the placenta. There were no major effects of restriction on fetal body, tissue or organ growth, except for the gastrointestinal tract (GIT). Total GIT weight was lower in restricted fetuses than in controls. More specifically, it was growth of the small and large intestine which was compromised. Small intestinal weight was significantly lower, both in absolute terms and relative to body weight. The intestinal diameter and mucosal area were significantly lower in both small and large intestine of restricted fetuses. Maturation of enterocytes was also delayed in nutrient-restricted fetuses. In addition, there were focal lesions of the brush border present, indicating abnormal epithelial differentiation. By term, in growth-retarded fetuses, growth deficits in many organs were present, including the GIT. The present study suggests that GIT growth deficits may have a long-term etiology, including at their onset, abnormal cellular differentiation. These results could explain why GIT function in intrauterine growth-retarded infants is more likely to be compromised than in premature or term infants.

Regulation of gastrointestinal growth in fetal sheep by luminally administered insulin-like growth factor-I.

Fetuses swallow large volumes of amniotic fluid. Absence of swallowing results in gastrointestinal tract (GIT) growth deficits. While it is not yet known to what extent the growth factors present in amniotic fluid are involved in GIT ontogeny, milk-derived growth factors are considered to be important for neonatal growth. Our experiment tested the hypothesis that a luminal growth factor (insulin-like growth factor-I, IGF-I) can sustain or promote GIT growth in utero in a model of gastrointestinal tract growth retardation. Ten-day infusion of either human recombinant IGF-I or vehicle into twin fetal sheep at 80 days gestation via an indwelling esophageal catheter resulted in altered GIT growth. Weight of the forestomach and small intestine increased. Significant histological changes were noted in the proximal small intestine, i.e. the region most exposed to the luminal infusion. Mucosal tissues were reduced in size. While the enterocytes in the proximal small intestine were generally more mature with regard to the ontogeny of the apical endocytic complex (which is responsible for uptake and transport of whole peptides), there were also many abnormal cytological features present. These included the development of large lysosomal-like inclusion bodies and many surfactant-like particles within the apical cytoplasm. Plasma IGF-I levels were on average 20% higher in treated siblings, suggesting that luminal IGF-I crossed the fetal gut and entered blood. IGF-II levels were not significantly affected. These observations are consistent with the suggestion that growth factors, which are present in swallowed amniotic fluid, influence fetal ontogeny.