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)

Unsuspected bacterial contamination of the small intestine was indicated by breath hydrogen testing in nine patients aged 2 to 34 months during physical examinations for chronic diarrhea and abdominal pain. Elevated bacterial counts of questionable significance were found in duodenal aspirates before and after antibiotic treatment. There was no evidence of bile salt deconjugation or structural changes in the small intestine by light or electron microscopy. This may indicate that the site of colonization is distal to the biopsy site. Breath testing indicated lactose malabsorption in all patients, and four of five patients tested also malabsorbed sucrose. Duodenal disaccharidase levels in all patients were within the normal ranges, but in eight patients the lactase-sucrase ratio was greatly elevated (0.80 +/- 0.36; normal less than 0.45). Dietary restriction alone did not cause complete cessation of symptoms, whereas all patients responded dramatically to oral antibiotic therapy. When patients were well, the lactase-sucrase ratio had returned to normal in those tested, and all nine had normal lactose and lactulose breath hydrogen tests. Unsuspected bacterial contamination of the small intestine, which is easily detected using the breath hydrogen test, may be more commonly associated with chronic diarrhea in children than has been previously realized. In such cases, therapy should be directed at removing the contamination.
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PMID:Bacterial contamination of the small intestine as an important cause of chronic diarrhea and abdominal pain: diagnosis by breath hydrogen test. 643 89

Patients undergoing massive small bowel resection for a variety of conditions develop severe nutrient malabsorption which gradually improves through mucosal hyperplasia in the remaining small intestine. Following massive small bowel resection, patients are generally fed elemental diets, often containing high concentrations of medium-chain triglycerides. We evaluated the effect of high percentage medium-chain triglyceride feeding on mucosal adaptation following massive small bowel resection in rats. Twenty 150-g Sprague-Dawley rats were subjected to 60% jejunoileal resection. Another 20 animals received sham operations. One-half of each group were fed a diet containing 83% of the fat as medium-chain triglycerides, the remainder were fed a diet containing 40% medium-chain triglycerides. Animals were pair-fed for 2 wk and subsequently killed. The remaining bowel was removed and unidirectional glucose and leucine uptake were measured using isolated sacs. Mucosal wet weight, protein, and sucrase content were determined. Animals fed medium-chain triglycerides demonstrated decreased mucosal weight in the proximal bowel, decreased mucosal sucrase activity in the proximal bowel, and decreased mucosal leucine uptake in the distal bowel. While medium-chain triglycerides offer an advantage to patients with short bowel syndrome because they are easily absorbed, they may not stimulate the same degree of mucosal adaptation following resection as long-chain triglyceride feedings.
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PMID:Effect of high percentage medium-chain triglyceride diet on mucosal adaptation following massive bowel resection in rats. 644 Oct 12

The pathogenesis of diarrhea caused by rotavirus infection was studied in miniature swine piglets. The animals were inoculated orally with 2 X 10(7) plaque-forming units of porcine rotavirus (OSU strain). During the height of diarrhea, intestinal function was investigated by in vivo perfusion of a 30-cm segment of proximal jejunum and a 30-cm segment of distal ileum. Absorption of Na+ and water decreased and 3-O-methylglucose transport was markedly reduced, P less than 0.01 compared to control animals. Mucosal lactase and sucrase levels were depressed in both the jejunum and ileum, P less than 0.001. Na+,K+-ATPase activity was significantly depressed only in the ileum, P less than 0.001. These changes were associated with a marked reduction in villous height, suggesting that the diarrhea could be an osmotic diarrhea due to nutrient (carbohydrate) malabsorption. Fresh stool samples were obtained and analyzed immediately for NA+,K+, osmolarity, glucose, and lactose; the osmotic gap was also determined. Stool osmolarity continually increased from 248 +/- 20 mosm/liter prior to inoculation to 348 +/- 20 mosm/liter at 75 +/- 1 hr postinoculation (P less than 0.005); the majority of the fecal osmotic gap could be accounted for by the amount of lactose present in the stools. Stool sodium increased from 34 +/- 6 mM prior to inoculation to a maximum of 65 +/- 4 mM at 53 +/- 1 hr postinoculation, P less than 0.001. There was no significant change in potassium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of rotavirus-induced diarrhea. Preliminary studies in miniature swine piglet. 648 82

There are at least 20 rare autosomal recessive disorders that are excessively common in Finland of which congenital lactase deficiency is one. During the last 17 years we have found 16 cases. In each case the mother noted watery diarrhoea, generally after the first feed of breast milk, and at the latest, by age 10 days. The lactose malabsorption was verified at a mean age of 36 (range 3-90) days, by which time the infants were dehydrated and 15 of them weighed less than at birth (mean weight for age was -2.8 SDs). On a lactose-free elimination diet (a group of 6 on Nutramigen and a group of 10 on soy-based formula) the children caught up in growth. One infant in each group showed allergic symptoms. While the infants were being breast fed their faeces contained 20 to 80 g/l lactose. In 24 peroral lactose tolerance tests, the greatest rise in blood glucose concentration was 0.8 mmol/l. Only 2 patients showed abnormal absorption when tested within a week of lactose elimination, and in each absorption tests became normal during the elimination period. Slight to partial villous atrophy of the jejunum was present in 4 early specimens, but in later ones the mean villous height was normal. The mean height of the epithelial cells was reduced and there were fewer intraepithelial lymphocytes in patients. The lactase activities in jejunal biopsy specimens were lower than in most patients with acquired lactase deficiency, with some overlap. The maltase and sucrase activities were normal.
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PMID:Congenital lactase deficiency. A clinical study on 16 patients. 684 26

It is well established that Giardia infection causes malabsorption. However, the precise mechanism of such a malabsorption is not known. To investigate this, transport studies, using the tissue accumulation technique, were carried out in mice infected with G. lamblia obtained from human stools. There was a significant fall in the transport of D-glucose, L-alanine and glycine in the infected animals compared with the controls. Kinetics of the D-glucose and glycine transport system were examined by measuring the tissue uptake in the presence of different concentrations of the substrate. For glucose, the affinity constant (Km) for the transport site was the same (4 . 37mM) in normal and infected animals but the maximal transport rate (V max) was considerably reduced in infected animals (158 . 7 mu moles/hr/g tissue) compared with (357 . 1 microgram moles/hr/g tissue) in controls. Results with glycine were similar; the Km was similar in control and infected animals (5 . 7 mM) whereas the V max was reduced in infected animals (27 . 02 microgram moles/hr/g tissue) compared with controls (45 . 5 micrograms moles/hr/g tissue). Analysis of the intestinal enzymes showed a significant decrease in the levels of brush border sucrase, lactase and alkaline phosphatase in infected animals; the cellular enzymes, LDH, GOT and GPT remained unaffected. The observed aberrations in the transport functions and brush border enzymes suggest that G. lamblia causes malabsorption by damaging the epithelial membrane of the enterocyte.
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PMID:Transport studies and enzyme assays in mice infected with human Giardia lamblia. 717 14

Investigations of the small bowel mucosa by scanning and transmission electron microscopy are reported in two coetaneous children with giardiasis. Serum immunoglobulins and mucosal architecture by light microscopy were normal in both, as well as activities of lactase, sucrase, and maltase. One of the children had suggestive evidence of malabsorption. Scanning and transmission electron microscopic examination of biopsied mucosa of the child with malabsorption suggested the following: increased secretory activity in crypts and increased cell damage, producing excess mucus containing extruded cytoplasm. It is hypothesized that the physicochemical properties of the mucoid material permitted ready interaction with the mucosal surface, the biochemical qualities of which could have been altered by the presence of the parasites. Close adherence of this mucoid layer to the surface gave it the aspect of a pseudomembrane which, by covering wide areas of the mucosal surface, probably functioned as an effective luminal barrier for nutrients. This pseudomembrane was not seen by light microscopy. Excessive secretion of mucus, its physicochemical and immunologic properties, and mucus-mucosal surface interaction could have been engendered by genetic and environmental factors, which need further study. Although some mucus was present in the mucosa of the other child, it was confined to the base of the villi, and did not cover the mucosal surface. The presence of a luminal barrier (mucoid pseudomembrane) may be added to the list of mechanisms implicated in causing malabsorption in giardiasis.
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PMID:Malabsorption in giardiasis: presence of a luminal barrier (mucoid pseudomembrane). A scanning and transmission electron microscopic study. 718 28

The in vitro and in vivo production of hydrogen gas (H2) from various carbohydrates or proteins has been examined in normal rats and in rats infected with the nematode Nippostrongylus brasiliensis. Normal rat fecal homogenates were capable of producing H2 in vitro from glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate. Direct injection of glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate into the cecum of normal rats resulted in approximately twice as much H2 production in vivo than when these same carbohydrates or proteins were administered to the normal rats by gavage. Partial small intestinal villous atrophy was produced by infecting rats with the nematode N. brasiliensis. Impaired small intestinal cell function and evidence of malabsorption in the nematode-infected rats included: (a) decreased activity of intestinal cell lactase (-43%), sucrase (-33%), and alkaline phosphatase (-46%); (b) decreased gut sac uptake of 3-O-(methyl-3H]-D-glucose (-21%) or 1-[carboxyl-14C]-aminocyclopentane-1-carboxylic acid (-28%); and (c) increased (+ 64%-561%) 14CO2 production after D-[U-14C]xylose administration. These rats produced approximately twice as much H2 after gavage administration of glucose, sucrose, xylose, bovine serum albumin, or casein hydrolysate compared with normal rats. The present study suggests that H2 analysis may be useful in the evaluation of small intestinal malabsorption states in rats.
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PMID:Use of hydrogen gas (H2) analysis to assess intestinal absorption. Studies in normal rats and in rats infected with the nematode, Nippostrongylus brasiliensis. 728 87

An oral sucrose tolerance test was performed in a group of 103 children, aged between 3 months and 15 years because of episodic diarrhea and/or abdominal pains. Sucrose malabsorption defined as an abnormal increase in expired hydrogen, was found in only 3 children who suffered from congenital sucrase-isomaltase deficiency. This 1% incidence of sucrose malabsorption was lower than the incidence of lactose malabsorption found in this group (33%). Mean rise in blood glucose during the sucrose test was higher (3.4 +/- 1.4 vs. 2.4 +/- 1.2 mmol/l, p less than 0.0001) and the occurrence of false flat blood glucose curves was lower (3% vs. 12.8%, p less than 0.05) than during the lactose test. These findings are consistent with the higher sucrase activity in the small bowel mucosa compared to lactase. In contrast to the lactose tolerance test, sucrose tolerance test should not be used as a screening procedure for secondary disaccharidase deficiency in children.
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PMID:Diagnostic value of sucrose tolerance test in children evaluated by breath hydrogen measurement. 736 16

To determine the prevalence of short polymers of glucose and starch malabsorption caused by small intestinal glucoamylase deficiency in children with chronic diarrhea, we studied small bowel biopsy specimens from 511 children (aged 1 month to 9 years) with chronic diarrhea evaluated at 54 medical centers. Glucoamylase and disaccharidase (lactase, sucrase, maltase, and palatinase) enzyme assays were performed. Of the 511 children, 15 had glucoamylase deficiency. Six who had significant small intestinal mucosal injury and disaccharidase deficiencies were defined as having secondary glucoamylase deficiency; the other nine patients with normal mucosal morphologic features were defined as having primary glucoamylase deficiency. Secretin tests showed normal pancreatic amylase values for age in all seven children tested. Four of them had abnormal findings on tolerance tests for starch and short polymers of glucose (rise in blood glucose concentration: < 20 mg/dl) and reducing substances in stools, and three of these four had symptoms of intolerance (abdominal distention, flatulence, and diarrhea). All seven patients responded to a starch elimination diet. After reintroduction of a starch diet, diarrhea recurred in four patients; this was alleviated 48 hours after reelimination of starch. We conclude that intestinal glucoamylase deficiency is present in some patients with chronic diarrhea.
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PMID:Small intestinal glucoamylase deficiency and starch malabsorption: a newly recognized alpha-glucosidase deficiency in children. 815 67

Human immunodeficiency virus (HIV)-associated intestinal abnormalities can occur before immunodeficiency or infection with opportunistic enteropathogens. Rhesus macaques infected with simian immunodeficiency virus (SIV) develop an AIDS-like illness that frequently includes enteropathy. The development of enteropathy and its association with SIV infection in the intestinal tract was examined. By 1 week after infection, SIV-infected macrophages and T lymphocytes were detected in gut-associated lymphoid tissue. In contrast to findings in the asymptomatic stage, SIV-infected macrophages were numerous in primary and terminal stages of infection. An acute enteropathy syndrome was observed in the primary acute stage of infection. Functional abnormalities of absorptive epithelium, indicated by D-xylose malabsorption and decreased sucrase activity, occurred before the onset of diarrhea or opportunistic enteric infections. These findings indicate that macrophages and T cells in the intestinal tract are early targets of SIV infection and may play a critical role in the development of SIV-associated intestinal dysfunction.
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PMID:Primary acute simian immunodeficiency virus infection of intestinal lymphoid tissue is associated with gastrointestinal dysfunction. 816 4


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