Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitamin A-deficient children, increased rates of bacterial infections in the intestine have been observed. The adherence of bacteria is a prerequisite for invasion. Thus, the effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes was studied. Male weanling rats matched by weight were divided into three groups: one group was fed a vitamin A-free diet for 8-12 weeks; another was given the same diet supplemented with retinol acetate; a third group matched for age served as controls. The vitamin A-deficient group showed a significantly lower growth rate and lower serum retinol levels than either the retinol acetate-supplemented or control groups. In all the groups, S. typhimurium possessing mannose-sensitive fimbriae adhered to enterocytes in significantly larger numbers than the nonfimbriated strains. The number of fimbriated S. typhimurium bound to enterocytes from the proximal small intestine was significantly higher in the vitamin A-deficient rats than in the pair-fed vitamin A-supplemented group (19.3 +/- 14.9 versus 7.8 +/- 5.0; p less than 0.05) or the control group (19.3 +/- 14.9 versus 8.7 +/- 3.5, p = 0.01). The specific activities of the enterocytes lactase, sucrase, and maltase and the protein content in the vitamin A-deficient rats were similar to those in the controls. These results demonstrate that vitamin A deficiency in rats is associated with the increased ability of S. typhimurium to adhere to proximal small intestinal enterocytes. However, the possible changes in the membrane of the enterocyte do not include decreases in brush border disaccharidases or protein content.
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PMID:Effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes. 197 42

The effect of vitamin A deficiency on the intestinal absorption of nutrients and the activities of brush border enzymes were studied in albino rats. Intestinal uptakes of D-glucose, L-methionine, L-tryptophan and L-histidine were significantly greater in vitamin A-deficient animals than in controls. The specific activities of total adenosine triphosphatase (ATPase), ouabain-sensitive ATPase, maltase and sucrase in the intestinal mucosa of vitamin A-deprived rats were 121, 124, 131 and 134 per cent respectively, of the corresponding values in control animals. The DNA content of the small intestine in vitamin A-deficient rats was 36.5 per cent lower than in control rats. The stimulation in digestive and absorptive capacity appears to be an adaptive change in vitamin A-deficiency which decreases the intestinal cell population.
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PMID:Effect of vitamin A deficiency on rat intestinal digestive & absorptive functions. 253 19

This study investigated the effect of clinical and subclinical vitamin A deficiency on intestinal structure and function in rats. Weanling male rats fed a vitamin A-deficient diet (VA-) for 40-42 or 60-63 d were compared with rats either pair-fed (PF) or with free access to the same diet supplemented with vitamin A (VA+). A reference (REF) group was fed a standard rat diet. Weight began to plateau in VA- rats after 42 d, becoming significantly different from PF rats at 60-63 d (P < 0.02). Diarrhea did not develop in any study group. VA- rats had clinical signs of vitamin A deficiency in the 60-63 d study, but not in the 40-42 d study. However, serum and liver retinol concentrations were negligible in all VA- rats. VA- rats in the 60-63 d study had significantly reduced villus height (P < 0.02), and sucrase and maltase activities (P < 0.02) compared with PF rats. There were no differences between VA- and PF rats in mucosal wet weights, protein and DNA concentrations, thymidine kinase activity and glucose transport. No differences were detected in the 40-42 d study for any variable measured. Because clinical vitamin A deficiency in rats causes only mild changes in intestinal structure and function, it is unlikely that these alterations alone are responsible for the interactions observed in epidemiological studies between vitamin A deficiency and diarrheal disease.
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PMID:Vitamin A-deficient rats have only mild changes in jejunal structure and function. 868 43

Two studies were conducted to investigate whether vitamin A-deficient rats were more susceptible to intestinal injury caused by methotrexate (MTX), since vitamin A deficiency alone causes only mild changes to jejunal structure and function. Weanling male rats were fed a vitamin A-deficient diet (-VA) for 40-42 d and compared to rats either pair-fed (PF) or with free access (+VA) to the same diet. Drinking water of PF and +VA rats was supplemented with 37.5 microg (Study 1) or 75 microg (Study 2) vitamin A (Rovimix A 500W)/d. Rats in each group received MTX (-VAMTX, PFMTX, +VAMTX) or vehicle. MTX administration reduced intestinal mucosal wet weight, protein and DNA concentrations, and sucrase and maltase activities in -VA and PF rats (P < 0.02). In Study 1, -VAMTX rats developed a severe jejunal enteropathy and had a higher incidence of diarrhea (P < 0.005), greater weight loss (P < 0.005), more disruption of villus architecture (P < 0.0001) and lower disaccharidase activity (P < 0.007) than PFMTX rats. Similar results were observed in Study 2. Liver retinol concentration (but no other variable) was greater in rats receiving 75 microg vitamin A/d (P < 0.001) than in those receiving 37.5 microg/d. The interaction of vitamin A deficiency and small intestinal injury may explain the efficacy of vitamin A supplementation in preventing childhood diarrheal disease mortality in developing countries, and highlights the need for ensuring adequate vitamin A status in people worldwide with diseases and/or treatments which may injure the gastrointestinal tract.
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PMID:Vitamin A deficiency exacerbates methotrexate-induced jejunal injury in rats. 916

Weanling male rats fed a vitamin A deficient (VAD) diet were compared with rats fed the same diet supplemented with vitamin A. Half of the VAD group was repleted with vitamin A at the age of 70 days. There was a decline in weight in the VAD group after 45 days. Serum and liver retinol concentrations were negligible in the VAD groups at 70 days of age. These levels returned to normal in the repleted group within 20 days of supplementation. Histological observations in the intestinal tissues of the experimental animals exhibited reduced villus height (p < 0.05) compared with the vitamin A supplemented group (VAS), reduced number of mucous secreting goblet cells and total enterocytes. In addition, a significantly higher number of proliferating cells was found along the crypt. Disaccharidases (sucrase and maltase), peptidases (gamma GT) and alkaline phosphatase activities were markedly lower along the brush border (p < 0.05) in the VAD group compared to the VAS group. We also determined the total DNA, RNA and protein in the jejunal tissues per 0.1 mg/tissue in both groups. The RNA production per cell in the VAD groups was notably lower than that of the controls (p < 0.05). Our observation indicates that brush border enzyme levels are altered in animals with vitamin A deficiency, and that phenomenon is augmented when calculated per single cell. This change may be attributed to direct effects of vitamin A on the rate of proliferation and differentiation of the epithelial tissue along the jejunum rather than to gross structural changes along the small intestine.
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PMID:Effect of vitamin A on small intestinal brush border enzymes in a rat. 978 59