Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of amylase, alkaline phosphatase and lipase in the pancreas, in the mucosa and on the surface of small intestine (turned out segments) was studied for elucidating the effect of vitamin A deficiency on the synthesis of the studied enzymes and their translocation to the surface of glycocalix cell membranes. The activity of amylase is established to increase in the homogenate of the pancreas, intestine mucosa and on the surface of cell membranes. The activity of alkaline phosphatase and lipase in the homogenate of small intestine mucosa and in the pancreas lowers. The results obtained evidence for a disturbance in the intestine digestive function with vitamin A deficiency, the may be connected with the damage of the mucosa membrane structures as well as with a disturbance in the biosynthesis of the protein playing a decisive role in formation of secretory products in cells.
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PMID:[Study of hydrolase activity of rat small intestine mucosa with vitamin A deficiency]. 72 94

Epithelial cells from hamster small intestine, in short term culture, incorporated [carbinol-14C]retinol into a compound that is identical to synthetic retinyl phosphate, as judged by chromatography on DEAE-cellulose, silicic acid, and thin layers of silica gel. The biological compound displays the same absorption spectrum as does synthetic retinyl phosphate with a maximum at 325 nm. Hydrolysis with mild alkali yields anhydroretinol, as it does for synthetic retinyl phosphate, with absorption maxima at 388, 368, and 346 nm. Enzymic hydrolysis by alkaline phosphatase releases 9% of the radioactivity as [14C]retinol. Under the same conditions, 9% of synthetic retinyl phosphate is hydrolyzed to retinol. The biological compound was tested for biological activity. At a concentration of 5.5 x 10-8 M it was as active as retinol and retinyl phosphate in reversing keratinization induced in hamster tracheal epithelium by vitamin A deficiency. It is concluded that hamster intestinal cells synthesize retinyl phosphate.
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PMID:Isolation, characterization, and biological activity of retinyl phosphate from hamster intestinal epithelium. 93 56

A burned guinea-pig model (30 per cent body surface area) was used to study the effects of dietary vitamin A. Sixty-five female guinea-pigs were infused enterally via gastrostomy feeding tubes with identical formulate (175 kcal/kg/day, 20 per cent of calories as protein) containing varying amounts of vitamin A. Groups I, II, III and IV received formulae containing 0, 10,000 iu (approximately equivalent to the guinea-pigs' RDA), 50,000 iu (5 x RDA) and 250,000 iu (25 x RDA) of vitamin A per litre, respectively. After 14 days of tube feeding, the animals were killed. Group I animals had evidence of vitamin A deficiency including low haemoglobin levels, lower red blood cell counts and lower caecal mucosal weight. Findings of hypervitaminosis A were observed only in animals given the highest dose of vitamin A (25 x RDA). These were elevated serum alkaline phosphatase and complement C3 levels and enlarged adrenal glands. Group IV also showed defective cell-mediated immunity as reflected by reduced delayed cutaneous response to dinitrofluorobenzene. In a second experiment groups I, II, III and IV were given formulas containing 0, 1 x RDA, 5 x RDA, and 10 x RDA of vitamin A respectively for 14 days. Through postburn days 12 to 14 they were injected subcutaneously with 3 x 10(8) of Staphylococcus aureus once daily. On postburn day 15 the animals were killed and the numbers of viable bacteria at each injection site were counted. No significant differences were observed in viable bacterial numbers between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of vitamin A in enteral formulae for burned guinea-pigs. 212 24

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

The effect of vitamin A on chicken intestinal mucosal morphology and functionality was tested in relation to severe and mild vitamin A deficiency and vitamin A repletion. Compared with rats and mice, chickens have a very quick response to a deficient dietary intake. Severe vitamin A deficiency altered the small intestine of chickens at both the biochemical and the morphological levels. It caused the loss of mucosal protein, reduced villus height and crypt depth and diminished activities of disaccharidases, transpeptidase and alkaline phosphate (EC 3.1.3.1). The ratios RNA:DNA, RNA:protein and protein:DNA, and the DNA concentrations in 1 g intestinal tissue, together with morphological measurements, provided knowledge about the pattern of lesion. The results indicated that (1) lack of vitamin A influenced cellular hyperplasia as it caused an increase in DNA content and in the number of enterocytes per villus; (2) lack of vitamin A influenced cellular hypertrophy as it decreased the protein:DNA ratio. There was no difference in mucosal enzyme activity between the two deficient groups. The repletion group exhibited a remarkable increase in mucosal enzyme activity only 4 d after switching to the control diet. The evidence presented in our paper suggests that the low vitamin A supply interferes with the normal activity of chicken intestinal mucosa as it influences the processes of proliferation and maturation of enterocytes.
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PMID:Vitamin A deficiency induces morphometric changes and decreased functionality in chicken small intestine. 992 82

1. The effect of vitamin A on the small intestine was examined in vitamin-A-deficient meat-type chickens. 2. Maturation and activity of the small intestinal cells were assayed by detection of proliferating cells with proliferating cells nuclear antigen, goblet cells with Alcian blue, mature cells with alkaline phosphatase and extent of RNA expression with dot blot analysis. 3. Vitamin A deficiency caused hyperproliferation of enterocytes, a decrease in the number of goblet cells, decreased alkaline phosphatase activity and decreased expression of 2 brush-border enzymes. 4. Our findings suggest that the absence of vitamin A interferes with the normal growth rate in chickens because it influences functionality of the small intestine by altering proliferation and maturation of cells in the small intestinal mucosa.
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PMID:Vitamin A deficiency interferes with proliferation and maturation of cells in the chicken small intestine. 1112 81

Weight loss after biliopancreatic diversion or duodenal switch is due to decreased calorie absorption secondary to fat malabsorption. Fat malabsorption may also cause essential fat-soluble vitamin deficiencies, which may have severe clinical consequences and alter calcium metabolism. Serum vitamins A, D, E, and K, zinc, parathyroid hormone, corrected calcium, and alkaline phosphatase levels were measured in a cohort of patients who had previously undergone biliopancreatic diversion. Two bariatric surgery units were involved in the study: New York University School of Medicine (New York, NY), and the Wesley Medical Center (Brisbane, Australia). A total of 170 patients completed the study. The incidence of vitamin A deficiency was 69%, vitamin K deficiency 68%, and vitamin D deficiency 63% by the fourth year after surgery. The incidence of vitamin E and zinc deficiency did not increase with time after surgery. The incidence of hypocalcemia increased from 15% to 48% over the study period with a corresponding increase in serum parathyroid hormone values in 69% of patients in the fourth postoperative year. There is a progressive increase in the incidence and severity of hypovitaminemia A, D, and K with time after biliopancreatic diversion and duodenal switch. Calcium metabolism is affected with an increasing incidence of secondary hyperparathyrodisim and evidence of increased bone resorption in 3% of patients. Long-term nutritional monitoring is necessary after malabsorptive operations for morbid obesity.
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PMID:Serum fat-soluble vitamin deficiency and abnormal calcium metabolism after malabsorptive bariatric surgery. 1474 35