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

Cytokines play a central role in immune cell response, but they also participate in the maintenance of tissue integrity. Changes in the cytokine network of the pig gut may be expected at weaning, because abrupt changes in dietary and environmental factors lead to important morphological and functional adaptations in the gut. This study measured the gene expression of 6 inflammatory cytokines along the small intestine (SI) and the proximal colon in 28-d-old piglets (n = 45) at different time points (0, 1, 2, 5 and 8 d) postweaning, using RT-PCR. Villus-crypt architecture and enzymatic activities of lactase and sucrase in the SI were also examined. The results confirmed that weaning is associated with morphological and enzymatic changes in the SI. In addition, the data indicated that cytokine response in the gut could be divided into two periods: an early acute response (0 to 2 d postweaning) and a late long-lasting response (2 to 8 d postweaning). Between d 0 and d 2, the levels of IL-1beta, IL-6, and TNF-alpha messenger RNA (mRNA) increased. Marked upregulation of IL-1beta mRNA occurred in most parts of the intestine, whereas IL-6 and TNF-alpha mRNA markedly increased only at specific sites in the intestine. Between d 2 and d 8, the levels of IL-1beta, IL-6, and TNF-alpha mRNA rapidly returned to preweaning values, except that the level of TNF-alpha mRNA remained high in the distal SI. Levels of IL-12 subunit p40 (IL-12p40) and IL-18 mRNA also decreased, compared to those on d 0. Taken together, these results demonstrate that weaning in piglets is associated with an early and transient response in gene expression of inflammatory cytokines in the gut.
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PMID:Weaning is associated with an upregulation of expression of inflammatory cytokines in the intestine of piglets. 1498 61

Lactase-phlorizin hydrolase gene expression is spatially restricted along the anterior-posterior gut axis. Lactase gene transcription is maximal in the distal duodenum and jejunum in adult mammals and is barely detectable in the proximal duodenum. By contrast, pancreatic duodenal homeobox-1 (PDX-1) protein is expressed maximally in the proximal duodenum. This study aimed to determine the role of PDX-1 in regulating lactase gene promoter activity in intestinal epithelial cells. Caco-2 cells were cotransfected with lactase promoter-reporter constructs in the presence of a PDX-1 expression vector and assayed for luciferase activity. PDX-1 cotransfection results in repression of lactase promoter activity. Sequence analysis of the lactase promoter revealed a putative PDX-1 DNA binding site in the proximal 100-bp lactase gene promoter. EMSAs demonstrated that PDX-1 can interact with the lactase promoter binding site but not with a site in which the core PDX-1 binding sequence TAAT is mutated. Site-directed mutagenesis of the PDX-1 core binding site in the lactase promoter-reporter construct suggests that PDX-1 can function independently of DNA binding to its consensus binding site. Stable overexpression of PDX-1 results in repression of the endogenous human lactase gene in differentiated Caco-2 cells. Given the contrasting spatial expression pattern, PDX-1 may function to specify the anterior boundary of lactase expression in the small intestine and is thus a candidate regulator of anterior spatial restriction in the gut.
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PMID:Transcriptional regulation of the lactase-phlorizin hydrolase promoter by PDX-1. 1510 97

Lactase is a disaccharidase that is present in the brush-border membrane of the small intestine, hydrolyzes lactose to glucose and galactose, and is therefore important in milk-fed animals. Assays based on quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) in the bovine species have not yet been described. Therefore, we have developed an RT-PCR assay for the quantification of lactase mRNA levels and have tested its suitability in the bovine gastrointestinal tract of seven 5-d-old milk-fed calves. Primers for RT-PCR amplification of bovine lactase mRNA were designed in the 100% identical regions of species (rats, rabbits, humans) from which lactase sequences were available. Lactase mRNA was expressed relative to mean levels of 4 housekeeping genes (glyceraldehyde-3-phosphate dehydrogenase, beta-actin, ubiquitin, and 18S). The presence of lactase mRNA along the entire gastrointestinal tract was evaluated in samples that consisted of whole gut walls (mucosa plus submucosa). Furthermore, mRNA levels of lactase were measured in fractionized layers of jejunal and ileal mucosa (mainly containing villus tips or crypts) and ileal lamina propria (mainly containing Peyer's patches). Agarose gel electrophoresis of the lactase PCR product revealed a single band that corresponded to the single-amplified product as predicted by the melting curve analysis of the PCR. The amplified partial-bovine lactase sequence showed 87% similarity with human and rabbit sequences and 82% similarity with the rat sequence. Lactase mRNA was present in whole walls (consisting of mucosa and submucosa) of the entire small intestine, but was absent in esophagus, rumen, fundus, pylorus, and colon. Furthermore, lactase mRNA was detected in fractionized villus and crypt layers of jejunum and ileum, but levels were higher in the jejunum in villus than in crypt fractions. No lactase mRNA was detectable in the lamina propria fraction of the ileum containing mainly Peyer's patches. In conclusion, the developed RT-PCR method allows study of lactase mRNA levels.
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PMID:Real-time PCR quantification of bovine lactase mRNA: localization in the gastrointestinal tract of milk-fed calves. 1554 87

Necrotizing enterocolitis (NEC) is a major inflammatory disease of the premature human intestine that can be prevented by glucocorticoids if given prenatally before the 34th wk of gestation. This observation suggests that a finite period of steroid responsiveness exists as has been demonstrated in animal models. Human intestinal xenografts were used to determine whether a glucocorticoid responsive period exists in the developing human intestine. Developmental responsiveness was measured by lactase activity and inflammatory responsiveness by IL-8, IL-6, and monocyte chemotactic protein-1 (MCP-1) induction after an endogenous (IL-1 beta) or exogenous (LPS) proinflammatory stimulus, respectively. Functional development of ileal xenografts were monitored for 30 wk posttransplantation, and the lactase activity recapitulated that predicted by in utero development. Cortisone acetate accelerated the ontogeny of lactase at 20 wk (immature) but the effect was lost by 30 wk (mature) posttransplant. Concomitant with accelerated maturation, the IL-8 response to both IL-1 beta and LPS was significantly dampened (from 6- to 3-fold) by glucocorticoid pretreatment in the immature but not mature xenografts. The induction of IL-8 was reflected at the level of IL-8 mRNA, suggesting transcriptional regulation. The excessive activation of IL-8 in the immature gut was mediated by a prolonged activation of ERK and p38 kinases and nuclear translocation of NF-kappa B due to low levels of I kappa B. Steroid pretreatment in immature intestine dampens activation of all three signaling pathways in response to proinflammatory stimuli. Therefore, accelerating intestinal maturation by glucocorticoids within the responsive period by accelerating functional and inflammatory maturation may provide an effective preventive therapy for NEC.
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PMID:Glucocorticoid responsiveness in developing human intestine: possible role in prevention of necrotizing enterocolitis. 1559 89

To determine the effect of a transient doe-litter separation (48 h) on milk production and feed intake from 1 to 21 days post-partum, a control group (C) in which litters had free access to nursing, and a biostimulated group (B) in which litters were separated from their does from d 9 to d 11 post-partum were used. Total milk production was higher in (C) than in (B) does (5090+/-1.1 g vs. 4593+/-150 g, P < 0.05). On days 12, 13, 14 and 15 of the lactation period, milk production was 40% (P < 0.0001), 18% (P < 0.05), 15% (P < 0.05), and 15% (P < 0.01) higher in (C) than in (B), respectively. No significant differences were observed in feed intake during the period studied (7961+/-352 g in (C) does, and 7834+/-329 g in (B) does). After fasting, 11-day-old kits showed lower gut weight, body weight, empty stomach relative weight (RW), stomach content RW and small intestine RW (P < 0.05), but the differences disappeared at 21 days of age. A reduction in villous height (P < 0.065) was observed in separated kits at 11 days old compared to 9- and 11 -day-old control kits (579.0+/-28.4 vs. 664.64+/-27.6, and 724.33+/-24.1 microm, respectively), but no differences were observed at either 16 or 21 days of age. Specific jejunal lactase activity increased significantly in 11-day-old separated kits (P < 0.05). A significant increase in sucrase activity at 21 days in both groups (P < 0.05) was detected. In conclusion, a fasting period of 48 h at 9 days of age does not compromise the subsequent development of certain digestive parameters of young rabbits.
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PMID:Transitory disturbances in growing lactating rabbits after transient doe-litter separation. 1563 62

The effect of enteritis on the development of the small intestine was examined in newborn, colostrum-deprived piglets infected with a human isolate of Y. enterocolitica (serotype 0:3, biotype 4) soon after birth. The piglets were killed 3 days (n = 6) or 5 days (n = 8) after infection, or antibiotic therapy was commenced on day 5 and the animals killed on day 14 (n = 5). Compared with the non-infected controls, infected animals had reduced mucosal lactase and sucrase, but not maltase activity, while after antibiotic therapy, previously infected piglets had a lower lactase and a higher maltase and sucrase activity. Lactase activity was significantly reduced in the duodenum and jejunum, and mean values were lower in the ileum, but the difference did not reach significance; maltase activity was greater at all ages from the distal jejunum to the mid-ileum; sucrase activity was reduced in all segments up to day 5 but after antibiotic therapy was increased in the jejunum and appeared early in the ileum. Enzyme profiles were more mature along the crypt-villus axis in some segments of the intestine in previously infected piglets. Sodium-potassium-ATPase activity was unchanged. There was a reduced villus height:crypt depth ratio, crypt hyperplasia and increased crypt cell proliferation. Morphological maturation, indicated by loss of vacuoles and location of the nucleus at the base of the enterocyte, proceeded distally from the duodenum to ileum from 3 to 14 days of age when only the ileum remained immature. In infected piglets, there was reduced vacuolation and earlier location of the nucleus at the base of the cell in the distal intestine. Accelerated maturity of specific disaccharidases and enterocyte morphology in infected piglets appears to be due to physical damage to the mucosa resulting in faster proliferation of crypt cells and migration of enterocytes. It is suggested that this may reduce macromolecular internalisation and impair the ability to utilise dietary carbohydrate and may have long-term effects on growth and immunological responses of the gut.
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PMID:Impact of Yersinia enterocolitica enteritis on disaccharidase activity and small intestinal morphology in colostrum-deprived newborn piglets. 1603 44

Extrauterine growth restriction in preterm infants secondary to suboptimal nutrition is a major problem in neonatal intensive care units. Evidence is emerging that early growth deficits have long-term adverse effects, including short stature and poor neurodevelopmental outcomes. The parenteral route of feeding is essential to maintain nutritional integrity before successful transition to the enteral route of feeding is achieved. Nevertheless, early initiation of enteral feeding in sub-nutritional trophic quantity is vital for promoting gut motility and bile secretion, inducing lactase activity, and reducing sepsis and cholestatic jaundice. Results emerging from over sixty randomized clinical trials are available for providing a template on which feeding protocols can be based. Preterm breast milk expressed from the infant's own mother is the milk of choice. Supplementation with a human milk fortifier is necessary to optimize nutritional intake. Preterm formulas are an appropriate substitute for preterm human milk when the latter is unavailable. There are over ten systematic reviews of randomized controlled trials published by the Cochrane Library that addressed feeding strategies, but most do not address long-term outcome measures of clinical importance. There is an urgent need for large-scale, long-term randomized controlled trials to help evaluate metabolic, growth, and neurodevelopmental responses of preterm infants to earlier and more aggressive nutritional management.
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PMID:Extrauterine growth restriction in preterm infants: importance of optimizing nutrition in neonatal intensive care units. 1615 65

The small intestine matures from a primitive tube into morphologically and functionally distinct regions during gut development. Maximal expression of the genes encoding the digestive enzymes lactase-phlorizin hydrolase and sucrase-isomaltase is spatially restricted to distinct segments along the anterior-posterior axis of the small intestine and is temporally regulated during postnatal maturation. Transcription factors capable of interacting with the intestinal lactase and sucrase gene promoters are candidate regulators of spatio-temporal patterning during gut development and maturation. We aimed to quantitatively examine and compare the relative expression levels of a set of intestine-specific transcription factors along the anterior-posterior gut axis during postnatal maturation. Our analysis was focused on the transcription factors capable of regulating the intestinal lactase and sucrase-isomaltase genes. A real-time PCR protocol was used to quantitatively examine and compare spatially and temporally the relative transcript abundance levels for intestine-specific factors during postnatal intestinal maturation. Distinct spatial expressions patterns were detected along the length of the small intestine for PDX-1, Cdx-2, GATA-4, GATA-5, GATA-6, HNF-1alpha, HNF-1beta and CDP transcription factor genes. There is a general decline in transcript abundance for the factor genes during postnatal maturation. Defining the spatio-temporal expression patterns for intestine-specific transcription factor genes contributes to investigation of the roles that factor gradients play in mediating gut development and differentiation.
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PMID:Spatio-temporal patterns of intestine-specific transcription factor expression during postnatal mouse gut development. 1637 57

Lactase gene expression is spatiotemporally regulated during mammalian gut development. We hypothesize that distinct DNA control regions specify appropriate spatial and temporal patterning of lactase gene expression. In order to define regions of the lactase promoter involved in mediating intestine-specific and spatiotemporal restricted expression, transgenic mice harboring 100 bp, 1.3- and 2.0- kb fragments of the 5' flanking region of the rat lactase gene cloned upstream of a luciferase reporter were characterized. The 100-bp lactase promoter-reporter transgenic mouse line expressed maximal luciferase activity in the intestine with a posterior shift in spatial restriction and ectopic expression in the stomach and lung. The temporal pattern of expression mediated by the 1.3-kb promoter?reporter transgene increases with postnatal maturation in contrast with the postnatal decline mediated by the 2.0-kb promoter-reporter transgene and the endogenous lactase gene. The differential transgene expression patterns mediated by the lactase promoter fragments suggests that intestine-specific spatial and temporal control elements reside in distinct regions of the DNA sequences upstream of the lactase gene transcription start-site.
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PMID:Lactase gene promoter fragments mediate differential spatial and temporal expression patterns in transgenic mice. 1662 94

Probiotics are usually defined as microbial food supplements with beneficial effects on the consumers. Most probiotics fall into the group of organisms' known as lactic acid-producing bacteria and are normally consumed in the form of yogurt, fermented milks or other fermented foods. Some of the beneficial effect of lactic acid bacteria consumption include: (i) improving intestinal tract health; (ii) enhancing the immune system, synthesizing and enhancing the bioavailability of nutrients; (iii) reducing symptoms of lactose intolerance, decreasing the prevalence of allergy in susceptible individuals; and (iv) reducing risk of certain cancers. The mechanisms by which probiotics exert their effects are largely unknown, but may involve modifying gut pH, antagonizing pathogens through production of antimicrobial compounds, competing for pathogen binding and receptor sites as well as for available nutrients and growth factors, stimulating immunomodulatory cells, and producing lactase. Selection criteria, efficacy, food and supplement sources and safety issues around probiotics are reviewed. Recent scientific investigation has supported the important role of probiotics as a part of a healthy diet for human as well as for animals and may be an avenue to provide a safe, cost effective, and 'natural' approach that adds a barrier against microbial infection. This paper presents a review of probiotics in health maintenance and disease prevention.
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PMID:Probiotics and their fermented food products are beneficial for health. 1669 65


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