Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The survival and prognosis of the prematurely born human infant are dependent on a successful transition from the intrauterine to the extrauterine environment. This is largely a consequence of the maturation of sufficient gastrointestinal function to provide adequate nutrition. However, the gastrointestinal tract of the premature infant, and to some extent, of the full-term infant, may be unprepared to provide the requisite absorptive function. Data presented in this symposium emphasize the dissociations in the development of human gastrointestinal function. Morphological maturation is completed early in gestation while glucose absorption increases with gestational age. Sucrase and maltase activities appear early; lactase activity begins to increase at 30 weeks and increases steadily to term. The latter pattern is accompanied by increased production of cortisol and thyroid in the fetus. The intraluminal phase of fat digestion is immature even in the full-term neonate. Both pancreatic secretory function and bile salt metabolism mature postnatally. Despite this relative immaturity, breast milk fat is absorbed with great efficiency by the term infant, and breast milk provides other important influences on intestinal development: mitogenic factor, immunological support, control of intestinal flora. The goals of nutrition support of the premature infant have been to maintain intrauterine growth standards; yet premature infants receiving pooled breast milk from mothers at 40 weeks or more may be given too little protein for their needs. Human milk from mothers of premature infants may be a more appropriate nutrient source. Supplements with higher contents of amino acids may lead to amino acid imbalance or hyperammonaemia. Additional stresses and requirements are imposed by illness or congenital anomalies. While we must apply current research findings to clinical care, we must also extend our knowledge of extrauterine human development. The ultimate measure of success in this field will be the physical and neurological capacities of infants followed prospectively.
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PMID:The immature intestine: implications for nutrition of the neonate. 9 85

The "in situ" kinetic constants (app. Km and Vmax) of brush border neutral alpha-glucosidase (EC 3.2.1.20) and lactase/beta-glucosidase (EC 3.2.1.21) were determined 4,6 (only alpha-glucosidase), and 12 days after 60% proximal intestinal resection in rat ileum at the villus base and the transition zone between middle and upper villus third by use of a quantitative biochemical analysis of enzymes in tissue sections (section biochemistry). Sham-operated rats served as controls, and the kinetic data (means per rat, time and villus position) were compared (n = 4 animals in each experimental group) first by an overall factorial analysis of variance and thereafter in detail using nonparametric test procedures. Both enzyme activities exhibited a differential response: No changes of lactase/beta-glucosidase kinetics, but a significant decrease in both Vmax- and Km-values of neutral alpha-glucosidase, which was already fully expressed on day 4 after resection and confined to the apical villus region still implying a basoapical increase of Vmax and thus maintaining the normal activity gradient on a lower level. In conclusion, a complex pattern of enzymatic adaptation to proximal intestinal resection ensues in the hyperplastic ileal mucosa which cannot be explained simply in terms of the hypothesis of cellular immaturity.
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PMID:The adaptive response of disaccharidase activities at different sites along the villus epithelium after proximal intestinal resection in the rat. A microdensitometric study of enzyme kinetics. 641 38

The biologic clock that determines the temporal sequence of maturation of digestive and absorptive processes in the gastrointestinal tract is genetically predetermined, but may be modified by dietary, hormonal, or other factors. In general it may be said that the gastrointestinal tract of full-term neonates is capable of digesting and absorbing a nutritionally adequate quantity of dietary protein but capacity is limited. Very low birth weight preterm infants, who are surviving the early neonatal period in increasing numbers, have immaturity of a wide range of digestive and membrane-associated absorptive processes; in addition macromolecular absorption may be increased. Whether a limited capacity to digest food protein results in increased or altered antigenic stimulation of these immature infants remains speculative with present knowledge. Immaturity of intestinal lactase may lead to problems of lactose intolerance, but there is recent evidence that lactase activity may be inducible by milk feeding.
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PMID:Enzymatic maturation of the gastrointestinal tract and its relevance to food allergy and intolerance in infancy. 643 78

Ethanol consumption has a toxic effect on the epithelium of the small bowel, but enterocyte maturity is very difficult to measure under these circumstances. However, when ethanol intake is combined with enterectomy, enterocyte immaturity is greater, permitting an easier separation of these two effects. In a group of rats (13 male Wistar rats weighing approximately 220 g) fed a liquid diet containing 35% ethanol for 4 weeks after resection of the proximal jejunum, the residual small intestine brush border maltase, sucrase, and lactase activities were similar to those of a pair-fed control group (13 animals). However, alkaline phosphatase activity was decreased in the mucosa and in the enterocyte brush border, probably because of the lower activity of this enzyme in the jejunum-ileum remnant of the alcoholic group.
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PMID:Effect of chronic ethanol consumption on the activities of residual small bowel brush-border enzymes after proximal jejunum resection in the rat. 865 45

Intestinal epithelial brush border hydrolases are important and sensitive enzyme markers of gastrointestinal development and function. Little is know about the mechanisms that regulate the induction of these enzymes during human fetal development, as these events occur primarily in utero. The present work used ectopically grafted human fetal jejunal xenografts (median age,13.3 wk of gestation), maintained in severe-combined immunodeficient mice, to study the differential expression of five different hydrolases after 10 wk of xenotransplantation. The spatio-temporal distribution of brush border alkaline phosphatase, aminopeptidase-N, alpha-glucosidase, lactase-phlorizin hydrolase, and dipeptidyl peptidase IV enzyme activities were measured quantitatively using scanning microdensitometry along the crypt-villus axes of fetal, xenograft, and pediatric (median age, 34 mo) biopsies. Ectopic grafting of fetal jejunum closely recapitulated the development of these enzymes in utero, with alkaline phosphatase, aminopeptidase-N, alpha-glucosidase, and dipeptidyl peptidase IV enzyme activities closely matching the spatio-temporal distribution and levels recorded in pediatric duodenal biopsies. Lactase-phlorizin hydrolase was the only enzyme not to reach values recorded in pediatric brush border membranes, although activities were significantly (5.6-fold) higher than in pretransplanted fetal bowel. Human jejunal xenografts therefore demonstrate an appropriate developmental induction of brush border hydrolase activity and may represent a useful model to study trans-acting factors that promote human epithelial differentiation and function in vivo. Characterization of such agents may be of potential therapeutic use in the treatment of diseases associated with gastrointestinal immaturity, notably necrotizing enterocolitis.
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PMID:Developmental regulation of intestinal epithelial hydrolase activity in human fetal jejunal xenografts maintained in severe-combined immunodeficient mice. 1147 3

The gut of preterm neonates is colonised with a paucity of bacterial species originating more from the environment than from the mother. Furthermore, a delayed colonisation by bifidobacteria promotes colonisation by potentially pathogenic bacteria. This may contribute towards the development of neonatal necrotising enterocolitis (NEC). The physiopathology of NEC is still unclear but immaturity of the gut, enteral feeding and bacterial colonisation are all thought to be involved. None of the current preventive treatments are considered satisfactory. Modulating the autochthonous microflora by probiotics or prebiotics could be a more reliable approach to prevention. Using gnotobiotic quails as an experimental model of NEC we have shown that onset of intestinal lesions requires a combination of low endogenous lactase activity, lactose in diet, and colonisation by lactose-fermenting bacteria such as the clostridia. The protective role of bifidobacteria was demonstrated in this model through a decrease in clostridial populations and in butyric acid. Oligofructose dietary supplementation was shown to enhance this effect with an increase in the bifidobacterial level and consequently a greater decrease in clostridia. However, oligofructose was unable to promote a bifidobacterial acquisition when the microflora was initially deprived of this group. Nevertheless, oligofructose can act as an anti-infective agent and decrease the occurrence or severity of the lesions depending on the bacteria involved. According to these results and to the fact that oligosaccharides are a major component of breast milk, the addition of oligofructose in formula milks may be a nutritional approach to favouring colonisation by a beneficial flora.
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PMID:Oligofructose and experimental model of neonatal necrotising enterocolitis. 1208 21

Intestinal diseases in neonatal calves may be due to morphological and functional immaturity. We have studied histomorphology, crypt cell proliferation rates (based on incorporation of 5-bromo-2'-deoxyuridine into DNA), presence of apoptotic cells (based on terminal deoxynucleotidyl transferase-mediated X-dUTP nick end labeling), and brush border enzyme activities in preterm calves (277 d of gestation), euthanized on d 1 (P0) or 8 (P8), and in full-term calves (290 d of gestation), euthanized on d 1 (F0) or 8 (F8). Vacuolated epithelial cells were present in ileum of P0 and F0 but not in P8 and F8. During the first 8 d, villus sizes, crypt depths, and proliferation rates of crypt cells in the small intestine of preterm calves did not significantly change. In contrast, in full-term calves during the first 8 d, villus sizes in jejunum decreased, crypt depths increased in small intestine and colon, and crypt cell proliferation increased in duodenum and jejunum. Submucosal thickness in jejunum was highest in P0, but in ileum it increased with gestational age and feeding. Gestational age x feeding interactions indicated increased activities of aminopeptidase N and reduced lactase activities only in F8 and reduced dipeptidylpeptidase IV activities only in P8. In conclusion, in preterm calves the small intestinal epithelium was immature and brush border enzyme activities differed in part from those in full-term calves.
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PMID:Preterm as compared with full-term neonatal calves are characterized by morphological and functional immaturity of the small intestine. 1545 93

Colic is a common and distressing functional gastrointestinal disorder during infancy. It is a behavioral phenomenon in infants aged 1-4 months involving prolonged inconsolable crying and agitated status with multifactorial etiology. Colic can be considered as a benign, self-limited process because the baby normally grows and feeds even with transient irritable mood. Nevertheless, infantile colic is a common difficulty causing anxiety during parenthood and a recurrent reason for them to seek medical help, especially if it is the first child. The causes of colic can be classified as non-gastrointestinal or gastrointestinal. The former includes altered feeding techniques, modified child-parent relationship, immaturity of central nervous system, behavioral etiology, and maternal smoking or nicotine replacement therapy. Instead, the latter involves inadequate production of lactase enzyme, cow's milk protein intolerance, alteration of intestinal microbiota, gastrointestinal immaturity, or inflammation which causes intestinal hyperperistalsis due to increase in serotonin secretion and motilin receptor expression.Probiotics may play a crucial part in the manipulation of the microbiota. Probiotic administration is likely to maintain intestinal homeostasis through the modulation of permeability and peristalsis, influencing the gut-brain axis and inhibiting hypersensitivity. This is a decisive field in the development of preventive and therapeutic strategies for infantile colic. However, further studies are needed for each specific formulation in order to better characterize pharmacodynamic and pharmacokinetic properties and to evaluate their application as a possible preventive strategy if administered early during infancy against the later development of pain-related FGIDs.
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PMID:Preventing and Treating Colic. 3065 51