Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.26 (invertase)
4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six-week-old rats subjected to prenatal and postnatal dietary restriction (maternal and weanling intake = 50% that of controls) were studied. Compared with controls, malnourished rats not only had reduced body (78 +/- 12 vs 187 +/- 21 g) and organ weights (small intestine: 4.51 +/- 0.46 vs 9.89 +/- 0.61 g; colon: 0.75 +/- 0.08 vs 1.77 +/- 0.18 g; liver: 2.75 +/- 0.34 vs 9.13 +/- 1.33 g; pancreas: 0.78 +/- 0.14 vs 1.67 +/- 0.49 g) but also decreased body weight-length ratios (6.5 +/- 0.3 vs 10.8 +/- 1.4 g/cm) and serum albumin levels. The small intestinal mucosa was hypotrophic (protein-DNA ratio: 5.02 +/- 1.43 vs 8.82 +/- 0.68, malnourished vs controls, respectively) with reduced mucosal thickness, villus height, and crypt depth. Specific activities of lactase, maltase, and sucrase were diminished (53%, 66%, 54% of control values, respectively). Colonic mucosa was hypoplastic with decreased mucosal thickness and crypt depth. Liver and pancreas were both hypotrophic and hypoplastic. The findings suggest that, in contrast to colonic mucosa, pancreas, and liver, the small intestinal mucosa maintained cell number during prolonged prenatal and postnatal malnutrition.
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PMID:Biochemical and morphological changes in the digestive tract of rats after prenatal and postnatal malnutrition. 250 4

The effects of malnutrition on mucosal goblet cell mucin levels were studied in rats deprived of 50% of their daily intake, as judged by pair-fed, age-matched control animals, for 5 wk. Average daily weight gain was 0.7 g/day compared with 5.8 g in age-matched (AM) rats; final weight was 246 +/- 9 g compared with 406 +/- 4 g. Immunoassayable mucin, sucrase, protein, and DNA were assayed in mucosal scrapings from the proximal, middle, and distal segments of the small intestine in malnourished rats, AM rats, and a third group of low-weight, less mature (LM) rats. Total protein, total DNA, and protein-to-DNA ratios in malnourished rats were unchanged compared with AM control rats and often higher than levels in LM control rats. In malnourished animals, mucin concentration per milligram protein was significantly decreased below AM control animals in the upper two segments and below LM control animals in all segments. Mucin concentration per milligram DNA was significantly lower in malnourished rats than in all segments of both control groups. In contrast, sucrase activity per milligram protein or DNA was either unchanged or increased in the malnourished rats, indicating that the reduction in mucin concentration was selective and did not reflect all surface glycoproteins. Isolated mucins from malnourished and AM control rats were chemically similar, and the affinity and number of antigenic determinants were the same. Malnutrition therefore leads to an absolute decrease in intestinal mucin rather than reduced molecular antigenicity. Impaired capacity to maintain mucosal mucin content may be a factor in reducing intestinal resistance to enteric infection in malnutrition.
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PMID:Mucin depletion in the intestine of malnourished rats. 258 Apr 45

The interaction between malnutrition and exposure to a mucosal damaging agent, difluoromethylornithine (DFMO), was examined by monitoring the small-intestinal changes in weanling rats. Malnutrition as induced by the expanded-litter method resulted in severe reduction in body weights in the expanded litters as compared to normal litters. Subsequent treatment of malnourished and well-nourished pups with DFMO for 7 days resulted in decreases in small-intestinal weights and enzyme contents. A 2 factors (well-nourished and malnourished) by 2 factors (DFMO-treated and nontreated) analysis of variance showed no interaction between malnutrition and DFMO treatment in terms of food intake, total mucosal protein, and contents of enterokinase, leucine aminopeptidase and sucrase. Very slight and insignificant interactions (p less than or equal to 0.2) were found for body weights, intestinal weights and total DNA content. Only one parameter studied, the maltase content, showed significant interaction between malnutrition and DFMO treatment (p less than 0.05). Three weeks after the withdrawal of DFMO, essentially all the changes caused by DFMO recovered. But those changes caused by malnutrition did not, such that the malnourished group, whether treated with DFMO or not, still remained significantly less than the control group in their small-intestinal parameters. Analysis of variance showed no interaction between malnutrition and DFMO treatment in the recovery phase. The results suggest that malnutrition is a more important factor in determining the intestinal damage and that malnutrition in the immediate postnatal period does not increase the sensitivity of the small intestine to the damaging effect of DFMO.
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PMID:Interaction of malnutrition and difluoromethylornithine-induced intestinal mucosal damage: degree of severity and subsequent recovery. 285 68

The influence of vitamin D and C deficiency on the kinetic parameters of sucrase and alkali phosphatase activities was studied in the microsomal fraction of the small intestinal mucosa of guinea pigs. It was found that Km values for these enzymes did not depend on the animal providing with these vitamins. Deficiency of one of these vitamins did not influence sucrase activity, however, simultaneous elimination of vitamins D and C resulted in the activity rise by 92%. Alkali phosphatase and Ca-ATPase activities proved to be similarly dependent on providing with vitamin D in the presence of vitamin C in the ration, while in the absence of vitamin C this dependence was not observed.
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PMID:[Enzymatic activity of the microsomal fraction of the mucosa of the small intestine in guinea pigs with vitamin D and C deficiencies]. 296 18

The reversibility of the effects of postnatal malnutrition on the intestinal brush border enzymes and somatic and intestinal weights were examined using either ad libitum or restricted feedings. Malnutrition was induced in the immediate postnatal period by expanding newborn rat litters to 20 pups/dam. At 21 days of age, malnourished pups exhibited significantly decreased body and intestinal weights as compared to those from control litters. Malnourished pups also had significantly elevated lactase specific activities whereas sucrase and maltase activities were not affected in the proximal small intestine. With subsequent nutritional rehabilitation by an ad libitum (food available 24 h/day) or restricted feeding regimen (food available 2 h/day), body and intestinal weights remained significantly depressed by 56 days in malnourished as compared to control animals. Rats on 2-h feedings consumed approximately 35% of the food consumed by their ad libitum-fed counterparts. Comparison of the ratio of weight gained to the amount of food consumed did not demonstrate a greater food efficiency with any particular feeding pattern. With ad libitum or restricted feedings, lactase specific activity in the proximal segment attained control values by 14 days. Restricted feedings resulted in an apparent elevation of specific activity of sucrase and of maltase, when rats were sacrificed at one chosen time point. Multiple time studies in a 24-h cycle showed that maximal elevations in enzyme activities were associated with feeding time. There were no significant differences in mean specific daily enzyme activities between the two feeding regimens. Restricted feedings show no advantage in enzyme efficiency or in promoting the rate of recovery of the intestine after postnatal malnutrition.
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PMID:Effect of nutritional rehabilitation on the development of intestinal brush border disaccharidases of postnatally malnourished weanling rats. 309 May 9

Although Strongyloides stercoralis is a common parasite, little is known about its effect on intestinal function. Published clinical studies are difficult to evaluate and compare because of the inability to differentiate the effects of the parasite load from that of various other coexisting features such as bacterial overgrowth, multiparasitism, malnutrition, or tropical sprue. Using a rat model where these problems do not occur, we found that Strongyloides ratti did not inhibit intestinal function in the healthy rat. In fact, in normal rats S. ratti appeared to increase ileal sucrase activity. In contrast, in the methylprednisolone-treated rat, S. ratti produced a decrease in lactase and sucrase activity and an increase in alkaline phosphatase activity. S. ratti had no effect on 3-O-methylglucose uptake or D-xylose absorption in either group. These results suggest that S. ratti has little effect on small bowel function in a healthy rat but can cause minor alterations in intestinal function in an immunosuppressed, methylprednisolone-treated, malnourished host. These results are also consistent with clinical observations seen with S. stercoralis in humans and with another nematode, Ascaris suus, in the pig model.
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PMID:Effect of Strongyloides ratti on small bowel function in normal and immunosuppressed host rats. 313 82

We studied lactase, maltase, and sucrase activities in the mucosa of self-filling blind loops (SFBL) in adult rats at weekly intervals after SFBL formation in order to determine the sequence in which disaccharidase activities fall. The studies were carried out on nourished and malnourished rats and extended to a recovery period induced by antibiotics to determine the effects of malnutrition on the establishment and repair of disaccharidase deficiencies caused by bacterial overgrowth. Malnutrition was produced by feeding 50% of the intake of paired rats fed ad libitum. Disaccharidase activities were determined in SFBL from nourished and malnourished rats at 7-day intervals until pandisaccharidase deficiency was established and during a 2-wk recovery period induced by antibiotics. Maximal SFBL bacterial counts in both nourished and malnourished groups of rats and brush-border glycoprotein degradation ratios were established at 7 days. In nourished rats only lactase was deficient at 7 days; maltase and sucrase fell later and sequentially. In malnourished rats all three disaccharidases were reduced at 7 days. Disaccharidase activities in self-emptying blind loops (SEBL), used as operated controls, were not decreased 28 days after surgery. Malnutrition had no effect on disaccharidase activities in the SEBL, and malnutrition did not affect recovery rates with antibiotic therapy. We conclude that small intestinal bacterial overgrowth causes a staggered loss of disaccharidase activities beginning with the loss of lactase activity. In the presence of bacterial overgrowth, malnutrition accelerates the conversion of a mono- to a pan-disaccharidase deficiency.
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PMID:Sequential disaccharidase loss in rat intestinal blind loops: impact of malnutrition. 315 66

The effects of malnutrition on the gastrointestinal tract have been previously investigated in animal models using dietary protein restriction. Because malnutrition is clinically a consequence of reduced dietary intake of all macronutrients, we investigated the effect of restricting a balanced diet on intestinal disaccharidases and histologic conditions of rats. Our diet-restricted animals gained less weight (13 +/- 9 gm) than the control animals (158 +/- 27 gm) over the 5-week study. The proximal, middle, and distal small intestinal segments from the experimental animals had reduced mucosal protein content (15 +/- 4 mg vs. 24 +/- 7 mg). In these segments the total amount of maltase was slightly decreased, whereas sucrase and lactase activities were normal or increased. The intestinal villus/crypt ratios were similar in the experimental and control animals. Mucosal cell height was significantly reduced in the diet-restricted groups; however, cell width was normal. We conclude that severely diet-restricted animals have mucosal protein loss caused in part by reduced cell height, but that the disaccharidase enzyme activities are normal. Diet-restricted animals appear to have sufficient intestinal enzymes to support a normal amount of disaccharide hydrolysis.
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PMID:Effect of restricting a balanced diet on rat intestinal disaccharidase activity and intestinal architecture. 357 3

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

To determine whether zinc has a specific role on intestinal growth and function, three groups of male weanling Sprague-Dawley rats were fed a semipurified zinc-deficient diet: ad libitum fed group received powdered diet and water containing 25 ppm of zinc; force fed (ZN, ZD) groups were fed identical amounts of diet to the ad libitum fed group by intragastric infusion three times per day. The diets were aqueous suspensions made with either deionized water (ZD) or water containing 25 ppm of zinc (ZN), and additional drinking water with (ZN) or without zinc (ZD) was offered ad libitum. Rats were sacrificed after 8 days of feeding. The ZD group showed growth arrest, perioral and periorbital dermal lesions, and abdominal distention within 8 days of feeding. Mucosal DNA, protein, sucrase, maltase, lactase, leucine aminopeptidase, and alkaline phosphatase were significantly decreased in the ZD group, whereas intestinal length, weight, and mucosal weight were unaltered. These results suggest that short-term isolated zinc deficiency impairs growth, digestion, and absorption in the rat small intestine, even in the absence of associated protein calorie malnutrition.
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PMID:Effects of short-term isolated zinc deficiency on intestinal growth and activities of several brush border enzymes in weaning rats. 408 Apr 54


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