Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulinlike growth factor-I (IGF-I) has been found in the milk of various species. To investigate if milk-borne IGF-I has any effect on postnatal gut development in neonatal animals, newborn rat pups were given orally 1 microg recombinant human IGF-I daily for 3 days. For comparison, a separate group of newborn pups was given 150 microg hydrocortisone, the hormone known to stimulate intestinal maturation in neonatal rats. Oral IGF-I treatment had no significant effect on the animal body weight nor on the weight of the stomach, small and large intestines, and pancreas. Oral administration of hydrocortisone significantly reduced body weight gain, but it had no apparent effect on internal organ weights. Both IGF-I and hydrocortisone treatments, however, significantly increased lactase, maltase and sucrase activities and hydrocortisone significantly increased aminopeptidase activity at the proximal small intestine when compared with the control. The finding supports the hypothesis that milk-borne IGF-I may play a role in regulating postnatal gut development in the suckling young.
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PMID:Oral insulinlike growth factor-I stimulates intestinal enzyme maturation in newborn rats. 920 Jun 69

In this study we investigated whether brain-gut peptides are implicated in the activation of the hypophysial-adrenal axis (HAA) in suckling rats treated orally with spermine. The first group of rats received i.p. injections of bombesin, vasoactive intestinal polypeptide (VIP), somatostatin or neurotensin, starting on day 11 of life, and killed on day 14. The small intestine was removed and analysed for its content of proteins, DNA, polyamines and for its specific activity (SA) of disaccharidases. The second group of rats received one of the hormones cited above and was killed 45 min after the treatment for determination of corticosterone plasma concentration. Rats of the third group were adrenalectomised then treated with bombesin as the first group. The fourth group of rats was orally treated with spermine and sacrificed 2, 3, 4, 6 and 8 h thereafter for analysis of plasma and intestinal concentrations of bombesin. The i.p. injection of bombesin increased the sucrase and maltase SA in the whole small intestine, while it decreased the lactase SA in the distal part. Intestinal weight and length, contents of DNA, protein, spermidine and spermine, and corticosterone plasma levels were enhanced by bombesin treatment. Somatostatin, neurotensin and VIP were ineffective on all the parameters studied. Adrenalectomy, in bombesin-treated rats, decreased the sucrase and maltase SA in the whole intestine, and decreased the lactase SA in the proximal intestine. It has no effect on intestinal weight and length, and protein content. Oral administration of spermine had no effect on plasma concentration of bombesin, whereas it decreased the content of this peptide in the whole small intestine. It is possible that bombesin may control intestinal development in suckling rats and be a link between the ingestion of spermine and the liberation of corticosterone by the adrenal glands.
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PMID:Involvement of bombesin in spermine-induced corticosterone secretion and intestinal maturation in suckling rats. 920 97

To evaluate whether the small bowel can be distracted by mechanical stress in analogy to limb lengthening by osteodistraction, a gut-lengthening apparatus was designed. This distractor was placed at the antimesenterical side of a defined jejunum segment in rabbits. Distraction was performed by 1 mm lengthening of the distractor once daily using extracorporal screws. An effective gut lengthening was achieved of 9.9 +/- 0.5 mm (approximately 100%) within 3 weeks. Treated animals gained weight and remained in good general condition. Fasting plasma levels of cholecystokinin, neurotensin, glucagon-like peptide-1, gastric inhibitory polypeptide, and insulin remained unaffected. Postoperative factor XIII levels were significantly diminished and gastrin was elevated during gut distraction. DNA and protein concentrations in the mucosa of the distracted gut segments corresponded to controls. Mucosal lactase and saccharase activities were reduced. In the distracted bowel segments total tunica muscularis thickness was more than doubled due to muscle cell hypertrophy. In distracted segments villous width was increased. Detection of proliferating mucosal crypt cells utilizing BrdUrd labeling revealed no effects. In conclusion, small gut lengthening by mechanical distraction is possible without major changes in gut morphology. This technique may hint a novel experimental approach for the treatment of short bowel syndrome.
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PMID:Small bowel lengthening by mechanical distraction. 924 19

13C-labeled glycosyl ureides were recently proposed as a new marker of the orocecal transit time: after passing the small bowel the sugar-urea bond is split by bacterial allantoicase. Further degradation results in 13CO2 which can be measured in the exhaled breath. The aim of this study was to detect an eventual allantoicase-like activity in the human gut and to elucidate the metabolism of glycosyl ureides by human intestinal brush border enzymes. Biopsies of 15 duodenal specimen and 6 colon specimen were homogenised and incubated with several disaccharides and their corresponding disaccharide ureides under various experimental conditions. Hydrolysis of the sugar-urea bond could not be observed neither in the small bowel nor in the colon. However, the conjugation between the two sugars was split. In a modified Dahlqvist assay lactase showed the same kinetics with lactose and lactose ureide as substrates whereas maltose showed a significantly 2.6-fold higher affinity to maltase than maltose ureide (P < 0.001). No major difference between these two substrates could be detected when total maltase activity was inhibited by acarbose. In summary, the human gut tissue possesses no allantoicase-like activity. Therefore, glycosyl ureides seem to be appropriate substances to test the orocecal transit time.
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PMID:Metabolism of glycosyl ureides by human intestinal brush border enzymes. 930

Non-physiological amounts of oral polyamines have been reported to induce precocious gut maturation in rat pups. The aim of the present study was to investigate organ distribution and metabolic fate of orally administered stable-isotopically labelled polyamines in rat pups. Pups received tetradeuterium-labelled putrescine (Pu-d4; 3 mumol), spermidine (Sd-d4; 5 mumol), spermine (Sp-d4; 3 mumol), or physiological saline twice daily on postnatal days 7-10 or 12-15. They were killed on days 10 and 15. We determined activities of ileal lactase (EC 3.2.1.23), maltase (EC 3.2.1.20), sucrase (EC 3.2.1.48) and diamine oxidase (EC 1.4.3.6) and established villus and crypt lengths. Polyamines and their labelling percentages in organs were determined by GC and mass fragmentography. Treatments did not affect growth rate, but caused lower weights of liver, kidneys and heart. Maltase activity increased, lactase decreased, whereas sucrase and diamine oxidase did not change. Villus and crypt lengths increased. Organ polyamine pools were labelled to different extents. Irrespective of the orally administered polyamine, all organs contained Pu-d4, SD-d4 and Sp-d4. Administered Pu-d4 and Sd-d4 were recovered mainly as Sd-d4, whereas Sp-d4 was recovered as Sp-d4 and Sd-d4. Total polyamines in a caecum, colon and erythrocytes increased, but increases were only to a minor extent with regard to labelled polyamines. Our data confirm precocious gut maturation by exogenous polyamines. Putrescine appears to be limiting factor. The exogenous polyamines were distributed among all investigated organs. They are not only used for the synthesis of higher polyamines, but also retroconverted to their precursors. Changes in erythrocyte polyamine contents suggest precocious stimulation of erythropoiesis.
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PMID:Oral administration of deuterium-labelled polyamines to sucking rat pups: luminal uptake, metabolic fate and effects on gastrointestinal maturation. 938 89

The activity of lactase enzyme declines after weaning. This study was to investigate changes in the lactase expression in the whole gastrointestinal tract during the development and the possibility that this and activity can be induced by lactose. Expression of lactase protein in the gut of 1-12-weeks old rats was studied by immunocytochemistry. Possible induction was evaluated by immunohistochemical and biochemical techniques in 8-week-old rats after lactose challenge for seven days. Lactase immunoreactivity was detected only in the small intestine and it decreased 20% during the week after weaning. A steady level of 40% lower than in the sucklings was found in the adult rats. In the lactose-challenged rats the optical density of immunoreactivity increased by about 30% in those that consumed the highest concentration of lactose. In the proximal jejunum, elevation of the enzymatic activity was three-fold. In the rat lactase protein expression decreased rapidly after weaning and expression and activity were induced by lactose-rich diet, most notably in the proximal jejunum.
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PMID:Age and continuous lactose challenge modify lactase protein expression and enzyme activity in gut epithelium in the rat. 944 19

Gene therapy is usually reserved for severe and medically refractory disorders because of the toxicity, potential long-term risks and invasiveness of most gene transfer protocols. Here we show that an orally administered adeno-associated viral vector leads to persistent expression of a beta-galactosidase transgene in both gut epithelial and lamina propria cells, and that this approach results in long-term phenotypic recovery in an animal model of lactose intolerance. A gene 'pill' associated with highly efficient and stable gene expression might be a practical and cost-effective strategy for even relatively mild disorders, such as lactase deficiency.
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PMID:Peroral gene therapy of lactose intolerance using an adeno-associated virus vector. 977 39

Epidermal growth factor and related substances mediate their effects on epithelial cells through binding to high-affinity receptors (EGF-R) at their basolateral surface and it is hypothesized that this growth factor system play a major role in gut morphogenesis and maintenance. The current review emphasizes on analyzing the expression and the biochemical characteristics of EGF-R in human fetal gut segments and correlating the biological actions of EGF-R ligands. They appear to be primarily involved in the local regulation of epithelial cell proliferation in which EGF-R are abundant. Alternatively, EGF-R ligands exert some precocious maturative effects by increasing intestinal lactase activity and decreasing brush border hydrolases in colon while they down modulate the expression of segment-specific markers of terminal differentiation such as sucrase, trehalase and glucoamylase in the intestine and chief cell lipase in the stomach. Such effects are consistent with the identification of receptors at the surface of all epithelial cell types, illustrating the modulatory role of EGF on differentiated gut epithelial cells. Comparison with animal models illustrates similar biochemical properties of receptors and underlines physiological aspects specific to human gut development. The relevance for ligand heterogeneity is also discussed and tentatively associated with different delivery pathways or physiological responses.
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PMID:Ontogeny of EGF receptors in the human gut. 988 80

Several lines of evidence suggest an important role for insulin in the regulatory mechanism of rodent small intestinal development. To investigate its potential implication in human gut, the immunofluorescent localization of insulin receptors (IR) and the influence of insulin (30 microU or 3 mU/ml) on [3H]-thymidine incorporation and on lactase and alkaline phosphatase activities were studied in fetal jejunum and colon (14-19 weeks). We demonstrate the early presence of IR, mainly detected in the basolateral portion of enterocytes and colonocytes along the crypt-villus axis. Insulin increased [3H]-thymidine incorporation as well as epithelial labeling indices in cultured explants from jejunum and colon without affecting enzymic activities. This study establishes, for the first time, that insulin stimulates proliferation of epithelial cells expressing IR in both segments without affecting brush border hydrolases in the developing human gut.
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PMID:Insulin modulates cellular proliferation in developing human jejunum and colon. 992 1

We measured intestinal safety factors (ratio of a physiological capacity to the load on it) for lactose digestion in developing rat pups. Specifically, we assessed the quantitative relationships between lactose load and the series capacities of lactase and the Na+-glucose cotransporter (SGLT-1). Both capacities increased significantly with age in suckling pups as a result of increasing intestinal mass and maintenance of mass-specific activities. The youngest pups examined (5 days) had surprisingly high safety factors of 8-13 for both lactase and SGLT-1, possibly because milk contains lactase substrates other than lactose; it also, however, suggests that their intestinal capacities were being prepared to meet future demands rather than just current ones. By day 10 (and also at day 15), increased lactose loads resulted in lower safety factors of 4-6, values more typical of adult intestines. The safety factor of SGLT-1 in day 30 (weanling) and day 100 (adult) rats was only approximately 1.0. This was initially unexpected, because most adult intestines maintain a modest reserve capacity beyond nutrient load values, but postweaning rats appear to use hindgut fermentation, assessed by gut morphology and hydrogen production assays, as a built-in reserve capacity. The series capacities of lactase and SGLT-1 varied in concert with each other over ontogeny and as lactose load was manipulated by experimental variation in litter size.
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PMID:Ontogeny of intestinal safety factors: lactase capacities and lactose loads. 1007 Jan 36


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