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)

Jejunal mucosal function and structure was examined in 31 patients with ulcerative colitis and 29 patients with Crohn's disease with ileal, ileocolonic or colonic involvement; A significant reduction of the specific activity of disaccharidases (lactase, sucrase and trehalase) in jejunal mucosal homogenate occurred in patients with inflammatory bowel disease. Similarly, alkaline phosphatase was reduced in ulcerative colitis. Several dipeptidases such as glycyl-leucine, leucyl-glycine, glycyl-glycine and valyl-proline hydrolase activities were lower in patients with inflammatory bowel disease than in controls. Histological changes in jejunal mucosal biopsies occurred in 71% of patients with ulcerative colitis and 61% with Crohn's disease. These changes ranged from mild abnormalities of villus architecture to marked reduction of villus height. Most patients with a reduction in mucosal enzymes had concommitant morphological changes in jejunal mucosal biopsy. The results of this study indicate that functional and structural abnormalities of the jejunal mucosa frequently occur in patients with inflammatory bowel disease without radiologic evidence of proximal small bowel involvement.
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PMID:Abnormalities of jejunal mucosal enzymes in ulcerative colitis and Crohn's disease. 47 7

Adenocarcinomas of the colon arise from adenomatous polyps. We hypothesized that sucrase-isomaltase (SI), a glycoprotein hydrolase, found in normal small intestine, fetal colon, and colon carcinomas is a marker associated with progression of adenomatous polyps with dysplasia to adenocarcinomas. To examine this hypothesis, we performed immunostaining using a polyclonal antihuman SI antibody in 32 adenomatous polyps with varying degrees of dysplasia. In addition, sucrase enzyme activity was determined in three sets of simultaneously harvested polyps, cancer, and adjacent normal mucosa from the same patient. All severely dysplastic polyps (6/6) exhibited SI staining. Most polyps (85%) with 3+ staining (i.e., greater than 10% of polyp positive for SI) had severe dysplasia, whereas those with mild dysplasia had either 1% to 5% staining or no staining in 95% of the cases. These data indicate that the extent of SI immunostaining in polyps correlates with the degree of dysplasia (p = 0.0001). Sucrase-isomaltase activity in the polyps was 18.1 +/- 1.8 mU/mg (mean +/- SD); in adjacent carcinoma SI activity was 29.1 +/- 1.8 mU/mg. Adjacent mucosa showed no activity in all cases. In summary, our results suggest that SI expression correlates with the progression of dysplastic adenomatous polyps to carcinoma. Sucrase-isomaltase expression may be useful as a clinical marker to improve our prognostic capabilities in patients with dysplastic lesions of the colon, that is, inflammatory bowel disease.
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PMID:Sucrase-isomaltase: a marker associated with the progression of adenomatous polyps to adenocarcinomas. 169

Clinical differences between the two human intestinal mucosal folate conjugases were assessed by measurement of their activities in normal individuals and in patients with chronic diarrhea of differing causes. Intracellular folate conjugase (ICFC) was 15-fold more active than brush border folate conjugase (BBFC) in jejunal mucosa from seven obese patients undergoing elective gastric bypass surgery. The activity of ICFC was similar among normal volunteers and patients with diarrhea of unknown origin (DUO), gluten-sensitive enteropathy (GSE), inflammatory bowel disease (IBD), and the short bowel syndrome (IBD-SBS). By contrast, BBFC, sucrase, and lactase were decreased significantly in GSE, and BBFC was increased in IBD-SBS. The activity of BBFC correlated with lactase and with sucrase in the normal subjects and in patients with DUO, whereas no correlations were found with the activity of ICFC in any group. Our clinical studies confirm that ICFC and BBFC are different enzymes. ICFC is not affected by intestinal disease, whereas the activity of jejunal BBFC, like that of other brush border enzymes, is decreased by mucosal injury and is also capable of adapting to distal small intestinal disease or surgical resection.
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PMID:Clinical studies of intestinal folate conjugases. 308 71

We examined the small intestinal histology disaccharidase activities as well as the incorporation of [3H]thymidine into DNA of biopsies maintained in organ culture from seven children (ages 9 months to 5 years) receiving total parenteral nutrition (TPN). Three children suffered from inflammatory bowel disease and received TPN for one month (short term). Four required long-term TPN (> 9 months) for short-bowel syndrome. DNA was extracted from the samples following serial precipitation with perchloric acid. Results were compared to those from 22 age-matched children investigated for abdominal pain or chronic diarrhea. Short-term TPN resulted in slightly lower lactase, sucrase, and palatinase activities that were not statistically different from controls. Long-term TPN resulted in focal mild villus atrophy and a decrease in disaccharidase activity in two patients. Biopsies from long-term TPN patients incorporated less thymidine compared to those of controls (P < 0.001) when data was expressed per total biopsy (3.6 +/- 1.1 vs. 8.4 +/- 1.1 fmol) or per milligram of tissue (1.0 +/- 0.12 vs 2.7 +/- 0.7 fmol). The above data are in general agreement with the hypoplastic effect of TPN in animals. However, in children, much longer periods of TPN are required to realize the changes.
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PMID:Small intestinal mucosa changes, including epithelial cell proliferative activity, of children receiving total parenteral nutrition (TPN). 835 71

The use of probiotics to enhance intestinal health has been proposed for many years. Probiotics are traditionally defined as viable microorganisms that have a beneficial effect in the prevention and treatment of specific pathologic conditions when they are ingested. There is a relatively large volume of literature that supports the use of probiotics to prevent or treat intestinal disorders. However, the scientific basis of probiotic use has been firmly established only recently, and sound clinical studies have begun to be published. Currently, the best-studied probiotics are the lactic acid bacteria, particularly Lactobacillus sp. and Bifidobacterium sp. However, other organisms used as probiotics in humans include Escherichia coli, Streptococcus sp., Enterococcus sp., Bacteroides sp., Bacillus sp., Propionibacterium sp. and various fungi. Some probiotic preparations contain mixtures of more than one bacterial strain. Probiotics have been examined for their effectiveness in the prevention and treatment of a diverse spectrum of gastrointestinal disorders such as antibiotic-associated diarrhea (including Clostridium difficile-associated intestinal disease), infectious bacterial and viral diarrhea (including diarrhea caused by rotavirus, Shigella, Salmonella, enterotoxigenic E. coli, Vibrio cholerae and human immunodeficiency virus/acquired immunodeficiency disorder, enteral feeding diarrhea, Helicobacter pylori gastroenteritis, sucrase maltase deficiency, inflammatory bowel disease, irritable bowel syndrome, small bowel bacterial overgrowth and lactose intolerance. Probiotics have been found to inhibit intestinal bacterial enzymes involved in the synthesis of colonic carcinogens. There are many mechanisms by which probiotics enhance intestinal health, including stimulation of immunity, competition for limited nutrients, inhibition of epithelial and mucosal adherence, inhibition of epithelial invasion and production of antimicrobial substances. Probiotics represent an exciting prophylactic and therapeutic advance, although additional investigations must be undertaken before their role in intestinal health can be delineated clearly.
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PMID:The role of probiotic cultures in the control of gastrointestinal health. 1072 14

Lactase deficiency can lead to significant symptoms in the pediatric population. To date, few studies have examined the prevalence of enzyme testing-based lactase and other disaccharidase deficiencies (DDs) in pediatric patients undergoing upper endoscopic evaluation. The primary objective of this study was to determine the prevalence of selective lactase and other DDs amongst a large cohort of pediatric patients with and without inflammatory bowel disease (IBD: Crohn's disease and ulcerative colitis) via a chart review of 739 patients who underwent esophago-gastro-dudenoscopy EGD between April 2010 and August 2016. We identified 560 pediatric patients (ages 1-18 years) who underwent mucosal enzyme testing at the time of their EGD. The overall rate of lactase deficiency (LD) was 39%. LD positively correlated with age (p=0.00017), but there was no significant difference between age matched IBD and non-IBD patients (45% vs. 42% p=0.68). Four patients (0.17%) were found to have selective maltase deficiency. No selective sucrase or palatinase deficiency was identified. Statistically significant differences occurred in lactase deficiency amongst patients of different races. In conclusion, lactase deficiency is a relatively common finding in children undergoing EGD though at no increased rate amongst the IBD patient population. Disaccharidase testing should be considered in pediatric patients undergoing EGD.
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PMID:Selective lactase deficiency is common in pediatric patients undergoing upper endoscopy. 3103 35

Self-renewal and differentiation are essential for intestinal epithelium absorptive functioning and adaptation to pathological states such as short gut syndrome, ulcers, and inflammatory bowel disease. The rodent Slfn3 and its human analog Slfn12 are critical in regulating intestinal epithelial differentiation. We sought to characterize intestinal function in Slfn3 knockout (KO) mice. Male and female pair-fed Slfn3KO mice gained less weight with decreased food efficiency than wild type (WT) mice, with more pronounced effects in females. RNA sequencing performed on intestinal mucosa of Slfn3KO and WT mice showed gene ontology decreases in cell adhesion molecule signaling, tumor necrosis factor receptor binding, and adaptive immune cell proliferation/functioning genes in Slfn3KO mice, with greater effects in females. qPCR analysis of fatty acid metabolism genes, Pla2g4c, Pla2g2f, and Cyp3c55 revealed an increase in Pla2g4c, and a decrease in Pla2g2f in Slfn3KO females. Additionally, adipogenesis genes, Fabp4 and Lpl were decreased and ketogenesis gene Hmgcs2 was increased in female Slfn3KO mice. Sequencing did not reveal significant changes in differentiation markers, so qPCR was utilized. Slfn3KO tended to have decreased expression of intestinal differentiation markers sucrase isomaltase, dipeptidyl peptidase 4, villin 1, and glucose transporter 1 (Glut1) vs. WT males, although these trends did not achieve statistical significance unless data from several markers was pooled. Differentiation markers, Glut2 and sodium-glucose transporter 1 (SGLT1), did show statistically significant sex-dependent differences. Glut2 mRNA was reduced in Slfn3KO females, while SGLT1 increased in Slfn3KO males. Notch2 and Cdx2 were only increased in female Slfn3KO mice. Although Slfn3KO mice gain less weight and decreased food efficiency, their biochemical phenotype is more subtle and suggests a complex interplay between gender effects, Slfn3, and another regulatory pathway yet to be identified that compensates for the chronic loss of Slfn3.
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PMID:Schlafen 3 knockout mice display gender-specific differences in weight gain, food efficiency, and expression of markers of intestinal epithelial differentiation, metabolism, and immune cell function. 3126 May 7