Systemic and luminal influences on the perinatal development of the gut

Abstract

Summary At birth, the mammalian gastrointestinal tract (GIT) must be able to support a shift from mainly parenteral nutrition in the fetus (via the placenta) to enteral nutrition in the neonate. In the perinatal period the GIT therefore undergoes enhanced growth as well as morphological and functional differentiation, and this maturational programme is influenced by a complex interplay of local, systemic and luminal factors. This review shows how systemic and luminal factors may influence GIT development in the perinatal period of the pig and sheep, two long‐gestation species. Adrenocortical hormones play a pivotal role in the prepartum maturation of the GIT in addition to their better known effects on the development of many other tissues and body systems. More particularly, in the fetal pig and sheep, the prenatal development of gastric acid and gastrin secretion, and of GIT hydrolase activities (chymosin, pepsin, amylase, lactase, aminopeptidases) is influenced by Cortisol. Additionally, glucocorticoids exert effects throughout the GIT by influencing morphological, cytological, and functional differentiation. Since the GIT epithelial cells comprise a renewing cell population there are also changes in cell kinetics. In addition to systemic factors, the presence of growth factors, hormones and nutrients from swallowed amniotic fluid (fetus) and colostrum (neonate) may influence GIT development In utero, fetal fluid ingestion has been shown to modulate tissue growth, macromolecule and immunoglobulin transport, enterocyte differentiation, cell turnover and activity of brush‐border hydrolases. These effects may be mediated via regulatory peptides (e.g. insulin‐like growth factor I, gastrin‐releasing peptides, insulin, epidermal growth factor, gastrin). A physiological role of luminally derived growth factors is supported by a number of unique structural and functional adaptations of the GIT in the fetus and neonate (low luminal proteolysis, intestinal macromolecule transport). Thus, in the pig and sheep, both systemic and luminal factors appear to play critical roles in GIT development in the perinatal period.

Early-postnatal changes in adiposity and lipids profile by transgenerational developmental programming in swine with obesity/leptin resistance

“…The development of the liver is critical for enhancing hepatic glucogenic capacity during the nutritional transition from a continuous maternal supply of nutrients via the placenta to a more intermittent supply from the milk via the intestine after birth (Shelley 1961, Dawkins 1966, Trahair & Sangild 1997 and, therefore, adequate liver development favours postnatal growth (Antipatis et al 2000). It has been described that foetuses undergoing adverse nutritional conditions have a faster liver development through a 'liver-sparing effect' (Haugen et al 2005).…”

Breast-v.formula-feeding: impacts on the digestive tract and immediate and long-term health effects

“…Postnatal epithelial growth and development is poorly defined in humans. However, from animal studies, it appears that extensive changes occur in the small intestine and colon architecture as well as in the hydrolytic and absorptive functions during the postnatal period (24) .…”

Beta-catenin/TCF4 transactivates miR-30e during intestinal cell differentiation

“…Cortisol and thyroid hormones are essential in the maturation of fetal organs, tissues and molecular signaling, and glucocorticoids have been well characterized to stimulate intestinal maturation by influencing morphological, cytological, and functional differentiation [47, 48]. In our study, dexamethasone was used to elicit differentiation events in IEC-6 cells, and the treatment was able to upregulate gene markers for absorptive enterocytes (ALP) [49, 50], Paneth cells (Lyzs, Pglyrp1 and spink4) [15, 51], goblet cells (trefoil F3), and enteroendocrine cells (CCK and Collagen IV) [52, 53] (data not shown).…”