In addition, enteral provocation with polyamines (spermine) ( Reference Dufour, Dandrifosse and Forget 9 ), the lectin from red kidney beans, phytohaemagglutinin (PHA) ( Reference Linderoth, Biernat and Prykhodko 10 ) or pancreatic and pancreatic-like proteases ( Reference Prykhodko, Pierzynowski and Nikpey 11 ) has also been shown to induce precocious gut maturation. This shift in the epithelial features of the SI results in a markedly decreased permeability, that is, gut closure, with improved intestinal barrier function ( Reference Pacha 4, Reference Menard, Cerf-Bensussan and Heyman 6 ).ĭespite being genetically pre-programmed, gastrointestinal development can be induced 3–4 d before natural weaning (postnatal day 21) by removing the rat pups from their dam ( Reference Lee and Lebenthal 7 ) or by injecting the pups with corticosteroids ( Reference Martin, Wu and Walsh 8 ). During the maturation process at weaning, these immature fetal-type enterocytes are replaced by more differentiated adult-type enterocytes, which are FcRn-negative and non-vacuolated in the proximal and distal SI, respectively ( Reference Arevalo Sureda, Westrom and Pierzynowski 5 ). The selective uptake of milk antibodies (IgG) involves binding of IgG to the neonatal Fc-receptors (FcRn) in the proximal SI, whereas the non-selective uptake of macromolecules involves the supranuclear vacuoles in the digestive enterocytes within the distal SI.

In addition, the pancreas, an accessory organ of the gastrointestinal tract, is affected with increased production and secretion of digestive enzymes ( Reference Rakhimov, Karimov and Kurbanov 3 ).ĭuring the suckling period in rodents, the immature intestine is highly permeable allowing passage to the general circulation of intact milk-borne bioactive compounds by the highly endocytic SI epithelium ( Reference Pacha 4 ). This results in growth of the gastrointestinal organs and prominent shifts in the small intestinal (SI) structure and function. Digestive function is well suited to the milk diet after birth however, during the 3rd postnatal week, with the transition from milk to a solid food diet, that is, weaning, the maturation process markedly accelerates and is completed around postnatal day 25 ( Reference Walthall, Cappon and Hurtt 2 ). Gastrointestinal development in the rat progresses during the 1st few postnatal weeks, following changes in the diet and the gut microflora within the protective milieu provided by the maternal milk ( Reference Cummins, Steele and Labrooy 1 ). In conclusion, PHA and protease differed in their early effects on the intestinal barrier both exerted a blocking effect on epithelial endocytosis, whereas protease treatment alone temporarily increased epithelial leakiness, which seemed to be confined to the distal SI. Following protease treatment, fluorescence microscopy showed decreased vesicular uptake of FD70 in the proximal SI and increased epithelial fluorescence in the distal SI.

PHA treatment hindered the passage of fluorescein isothiocyanate-dextran (FD) 4 to blood, whereas protease treatment temporarily increased plasma levels of FD4, and the urine lactulose:mannitol ratio, indicating increased intestinal leakiness. Within 1 h of oral administration, both treatments prevented the absorption of macromolecules to blood that was observed in controls. A period of 24 h following oral administration, both PHA and protease provocation stimulated small intestinal (SI) growth and pancreatic secretion, as indicated by decreased pancreatic trypsin and increased luminal enzyme content. Intestinal in vivo permeability was assessed by oral administration of different-sized marker molecules and measuring their passage into the blood or urine 3 h later. The effects of oral administration of protease (trypsin) or PHA to 14-d-old suckling rats were studied during 24 h in comparison with water-fed controls. We investigated the early effects of gut provocation on intestinal barrier and pancreatic functions, to get a better understanding of the mechanisms that initiate gut maturation. Mimicking this, gut development can also be induced precociously, 3–4 d earlier than it would occur naturally, by enteral exposure to phytohaemagglutinin (PHA), or various proteases. Gut maturation naturally accelerates at weaning in altricial mammalian species, such as the rat.

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