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)

Rats were kept undernourished from birth to 24 days of age. At 17 days of age, the undernourished animals were divided into two groups and then injected with either saline or epidermal growth factor (EGF; 20 micrograms/kg) once a day for 7 days. They were killed 12-14 h after the last injection at which time the animals were 24 days old. During the experimental period the undernourished animals were prevented from weaning. A well-nourished group (weaned) which was injected with saline from 17 to 24 days of age, was also included. Undernutrition by itself significantly decreased body weight and the weight of the oxyntic gland area, antrum, and small intestine. This was also accompanied by a parallel reduction in DNA, RNA, and protein content in the oxyntic gland and small intestine. However, administration of EGF to undernourished rats resulted in a partial reversal of the situation. In undernourished rats, EGF caused significant enhancements in body weight as well as the weight of the gastrointestinal tissues and their protein and nucleic acid content when compared with the saline-treated undernourished controls. Furthermore, the magnitude of stimulation was found to be greater in the oxyntic gland than in the small intestine following EGF administration. The antral or serum gastrin levels were not affected by EGF. In both saline- and EGF-treated undernourished rats, lactase, sucrase, and alkaline phosphatase activities (expressed as total or specific activity) were found to be significantly higher than in the well-nourished animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postnatal undernutrition: effect of epidermal growth factor on growth and function of the gastrointestinal tract in rats. 620 84

The enzymatic activities of maltase, sucrase, and lactase were determined in jejunal biopsies obtained from 24 children with gastrointestinal symptoms and different degrees of protein energy malnutrition (PEM) to see if these differences were related to the extent of malnutrition or concomitant small intestinal mucosal injury. Even in patients with moderate PEM, lactase activities were significantly lower than control values. The decrease in lactase activity seemed to depend on the severity of malnutrition. In contrast, maltase and sucrase activities were decreased only in second and third degrees of PEM, while no significant changes were observed in first degree and marasmic kwashiorkor. Histologically, all children with PEM had grade I to II mucosal injury which did not correlate with the degree of malnutrition. These results indicate that PEM affects each of the disaccharidases of the jejunal mucosa differently, with lactase being most sensitive to PEM and reflecting most closely the degree of PEM. In contrast, morphological changes showed no correlation with the degree of PEM.
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PMID:Moderate and severe protein energy malnutrition in childhood: effects on jejunal mucosal morphology and disaccharidase activities. 641 68

A 90% jejunoileal bypass induces in the rat a protein malnutrition state which is characterized (1) by the decreased level of plasma proteins and albumins and (2) by the reduced level of most essential and non-essential plasma amino acids. In the exocrine pancreas there was a decreased content of digestive enzymes, especially of amylase, while the secretion of enzymes studied in vitro was reduced. In the ileum left in one piece, the specific activities of maltase and sucrase increased significantly while aminopeptidase was unaffected. It is suggested that exocrine pancreatic insufficiency observed after small bowel bypass in the rat might contribute to protein malnutrition (1) by producing maldigestion and (2) by inducing an imbalance in intestinal enzymes favouring a preferential absorption of carbohydrates compared to proteins, thus emphasizing the protein malnutrition state.
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PMID:Protein malnutrition after jejunoileal bypass in the rat. Possible contribution of the exocrine pancreas and the included intestine. 642 94

In vivo jejunal transport of amino acids, monosaccharides, sodium, and electrolytes were studied in rats made nephrotic with puromycin aminonucleoside (PAN) and in pair-fed controls. Studies were performed 14 days after a single intravenous dose of PAN when rats were no longer edematous, but were still hypoproteinemic. There was decreased absorption of glucose, 3-0-methyl glucose, glycine, phenylalanine, histidine, water, and sodium in the nephrotic animals but transport of fructose, lysine and potassium was similar in the nephrotic and control animals. Enzyme kinetic studies for glucose transport showed a mixed type of inhibition affecting both Vm and Km. The jejunal mucosa of nephrotic and control rats had similar ATP content and enzyme activity for lactase, sucrase, maltase and (Na-K)-ATPase and the ratios of RNA to DNA were similar in the nephrotic and control rats. No abnormality of the jejunum was detected by light or electron microscopy. The data suggest that the impairment of absorption is a result of decreased activity of jejunal membrane carrier mechanisms. The altered transport may be secondary to effects related to the metabolic consequences of nephrotic syndrome and does not appear to be related to acute purine aminonucleoside toxicity, edema or malnutrition.
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PMID:Jejunal transport in experimental nephrotic syndrome. 662 9

In infants suffering from protein-calorie malnutrition, the decreased intestinal mucosal lactase specific activity could be due either to the protein-calorie malnutrition or to the commonly associated enteritis (viral or bacterial) and intestinal parasites. We studied intestinal mucosal disaccharidase (lactase, sucrase, and maltase) specific activity in suckling (1 and 2 wk old), weanling (3 wk old), and postweaning (4 and 6 wk old) control and growth-retarded (malnourished) rats. Growth retardation was induced by feeding mother rats and postweaning rats a diet deficient in protein. In the malnourished rats, with few exceptions, specific activity of the disaccharidases in the intestinal mucosa were similar to those in the corresponding control groups of rats. However, because of marked mucosal atrophy total intestinal mucosal disaccharidase activities were more than 50% lower in the malnourished rats. These findings suggest that the specific activity of the intestinal mucosal disaccharidases is not affected by malnutrition per se.
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PMID:Intestinal disaccharidases in malnourished infant rats. 679 98

Previous work in our laboratory and in others suggest that protein malnutrition plays an important role in the pathogenesis of hepatic dysfunction after jejunoileal bypass for morbid obesity. This experimental study was undertaken to attempt to correlate hepatic dysfunction (the criterion used was the bromsulphalein clearance) to morphological and enzymatic adaptation of the functioning intestine in the rat. It was observed that the period of impaired bromsulphalein clearance is concomitant with a slight ileal morphological adaptation and especially with a period of selective adaptation of maltase and sucrase activities, whereas there is no increase in aminopeptidase activity. These data support the hypothesis that after jejunoileal bypass a preferential absorption of carbohydrates along with a protein deficiency state could occur and as in kwashiorkor it results in an impaired nutritional status, a major contributing factor to bypass-induced liver injury.
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PMID:Imbalance in brush border enzyme activities as a possible cause of hepatic dysfunction after jejunoileal bypass in the rat. 704 83

Deficiency of vitamin D, responsible for impaired absorption of calcium in rat small intestine, did not affect the activity of saccharase (marker enzyme of microvilli) in homogenate of intestinal epithelium and in an isolated fraction of microvilli. Content of lipid phosphorus per mg of protein in the microvilli of rats, deficient in vitamin D, was decreased by 30% as compared with the control animals. Deficiency of vitamin D was accompanied by alterations in ultrastructure of 10-15% of enterocytes from small intestine. These alterations consisted in more widely spaced arrangement of microvilli, their fragmentation into separate vesicles with liberation of apical cellular surface, swelling of mitochondria with reduction of their crysts, enlargement of rough endoplasmic reticulum cisterns. The layer of glycocalix on the microvilli was decreased or completely disappeared in most enterocytes. The impairments found in submicroscopic organization of enterocytes might constitute the morphologic basis for the disturbed calcium absorption in the intestine under conditions of vitamin D deficiency.
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PMID:[Duodenal enterocyte ultrastructure of rats fed different amounts of vitamin D]. 745 15

Previous studies in very young rats have shown that dietary nucleotides improve small intestine repair after injury or malnutrition. To investigate the potential effect of nucleotides in old rats, which have a diminished capability for intestinal repair, 17-mo-old rats were deprived of food for 5 d and then fed a nucleotide-free diet or a nucleotide-supplemented diet for 3 or 6 d. Intestinal jejunal and ileal mucosal weight, protein and DNA were evaluated as intestinal growth markers, and brush-border maltase, sucrase, lactase and aminopeptidase activities were evaluated as intestinal differentiation markers. The adenine nucleotide pool and the adenylate energy charge were also evaluated as indices of nucleotide availability. Food deprivation significantly decreased mucosal growth markers as well as differentiation markers in both jejunum and ileum. The ATP pool was also significantly depressed, but the adenylate energy charge was not significantly altered. To a certain extent, refeeding restored the losses, but in the rats that were fed the nucleotide-free diet, the restoration of the jejunum was significantly slower and the restoration of the ileum differentiation markers was incomplete compared with the rats fed the nucleotide-supplemented diet. The results suggest that dietary nucleotide intake in the elderly may accelerate the normal physiological intestinal response to refeeding after food deprivation.
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PMID:Dietary nucleotides accelerate intestinal recovery after food deprivation in old rats. 778 93

The jejunal disaccharidases, sucrase, maltase and lactase, were determined in jejunal biopsies obtained from 43 malnourished children and 10 controls. In the study group, 63% were girls and 93% had severe malnutrition. Lactase activity was significantly reduced in third and fourth degree malnutrition (p < 0.05 and p < 0.005, respectively), but maltase activity was significantly reduced only in the fourth degree malnutrition (p < 0.01). After recovery, maltase and sucrase activities showed a marginally significant increase (p = 0.06), where lactase showed no significant increase (p > 0.05). We conclude that jejunal disaccharidase activity decreases significantly with increasing severity of malnutrition, lactase being the most severely affected and the last to recover.
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PMID:Jejunal disaccharidases in protein energy malnutrition and recovery. 789 32

Mild to moderate protein energy malnutrition (PEM) was induced in young developing rhesus monkeys by giving them half of the casein-based synthetic diet which was given to control animals. After a body weight reduction of 30-40%, the PEM animals were sacrificed. The small intestine was removed, flushed with ice-cold saline, everted and divided into equal proximal, middle and distal segments. Brush border membrane vesicles (BBMV) were prepared from all three segments and assayed for marker enzymes, e.g. sucrase and alkaline phosphatase, to assess their purity. Sucrase was found to be purified 23-fold and alkaline phosphatase 12-fold compared to the respective homogenates in all three parts. In PEM animals, uptake of [U-14C]L-leucine into the BBMV was diminished in all three segments and cholesterol and phospholipid levels also decreased significantly. As a result there was an elevation in the molar ratio of cholesterol to phospholipid, and the sphingomyelin: phosphatidylcholine molar ratio also increased. This signified a decrease in lipid fluidity and amino acid uptake in PEM in the small intestine. Histologically, a mild to moderate grade of partial villus atrophy was observed in the intestine. The diminished uptake and lipid fluidity of the membrane and the histological changes returned to their control values after nutritional rehabilitation.
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PMID:Effect of protein energy malnutrition on the lipid composition and leucine uptake of small intestinal brush border vesicles of growing rhesus monkeys. 806 90


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