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)

The location of cell proliferation and differentiation in chicken small intestinal epithelium was examined using immunostaining, measurement of DNA synthesis and brush-border enzyme activities. Chicken enterocytes were removed sequentially from the villus using a modification of the Weiser (1973) method. Alkaline phosphatase activity was relatively constant along the villus tip-crypt axis but decreased in the crypt fractions, whereas sucrase and maltase activities showed higher activity in the upper half of the villus and lower activity in the lower half of the villus and in the crypt. Immunostaining of proliferating cell nuclear antigen indicated the presence of proliferating cells both in the crypt and along the villus, including some activity in the upper portion; the crypt region exhibited a significantly higher number of proliferating cells. Labelled thymidine incorporation into cell fractions after 2 h incubation exhibited a similar pattern of proliferation, with the most active region observed in the crypt and proliferation activity decreasing along the villus. However, some activity was found in the upper half of the villus. After 17 h incubation, cells from the middle region of the villi showed greater proliferation ability than the 2 h incubation. These results indicate that, unlike mammals, chicken enterocyte proliferation is not localized only in the crypt region, and that the site of enterocyte differentiation is not precisely localized.
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PMID:Cell proliferation in chicken intestinal epithelium occurs both in the crypt and along the villus. 964

The effects of the energy and purine content in the diet on mucosal cell mitosis, function, and apoptosis in the small intestine of pigs were investigated in two experiments. In experiment I, three groups of five pigs were first fed a commercial diet that contained 9.1 MJ metabolizable energy (ME) per kilogram dry matter (DM) and 16.4% crude protein. It was followed by the experimental diets for 5 days each starting with an energy deficit (5.8 MJ ME/kg DM; 7% crude protein) followed by a high-energy diet with low purine content (14.1 MJ ME/kg DM; 13.6% crude protein; 460 mg purines/kg), or alternatively an isocaloric high-purine diet (2,160 mg purines/kg). During experimental periods, blood samples were drawn daily through catheters for insulin-like growth factor-I (IGF-I) determination. The animals were killed at the end of the corresponding feeding period and gut tissue samples were collected. In tissue samples, IGF-I and parameters for the characterization of mitosis (thymidine kinase [TK], proliferating-cell nuclear antigen [PCNA]) and differentiation (RNA content, alkaline phosphatase, sucrase) were measured. The degree of apoptosis was determined histologically. In experiment II, five pigs were fitted with simple T-cannula at the distal jejunum. They were fed the three experimental diets consecutively for 7 days each and sucrase and alkaline phosphatase were measured in digesta (four samples daily). IGF-I in blood but not in tissue clearly responded to the energy content of the diet with a decrease during the deficit and an increase in the two high-energy groups. However, purines had no additional effect on IGF-I. TK, PCNA, and gut weight showed an energy effect on mitosis, which was paralleled by increased peripheral IGF-I. Purines led to a further increase of mitosis, but IGF-I and gut weight were not increased. The degree of mitosis was correlated with higher activities of sucrase and alkaline phosphatase and also with the number of apoptotic cells. The enzyme activity increased from the deficit to the high-energy group and was further elevated due to purines. The results from experiment II also confirm these effects of energy and purines, because the activities of the enzymes in digesta decreased during energy deficit, but increased due to energy and in addition to purines.
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PMID:Effects of energy and purines in the diet on proliferation, differentiation, and apoptosis in the small intestine of the pig. 975 Dec 40

The small intestine plays an important role in the digestion and absorption of many nutrients. To investigate the contribution of carbohydrate digestion to diabetes mellitus, we examined the morphological changes of the small intestine, and the expression of sucrase-isomaltase, which is one of the intestinal disaccharidases, in diabetic model rat, that is the streptozotocin-induced (STZ) diabetic rat (insulin-deficient model), and the Otsuka Long-Evans Tokushima Fatty (OLETF) rats and the Goto-Kakizaki (GK) rats (type 2 diabetic models). Intestinal hyperplasia was observed in STZ, OLETF, and GK rats. Moreover, in the small intestine of each diabetic strain, the proliferating cell nuclear antigen (PCNA)-labeling index, which is a marker of proliferation, was higher than in the respective control. Cdx1 and Cdx2, known to be transcriptional factors related to intestinal proliferation and differentiation, were more highly expressed in STZ, OLETF and GK rats than in the respective controls. These findings indicate that small intestinal hyperplasia, and thereby the resultant increase of total activity of disaccharidases such as sucrase and isomaltase in the entire small intestine, might be one of the reasons for postprandial hyperglycemia in diabetes mellitus.
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PMID:Morphological changes and increased sucrase and isomaltase activity in small intestines of insulin-deficient and type 2 diabetic rats. 1294 Apr 55

Currently 15% of U.S. infants are fed soy formulas that contain up to 14 mg of genistein equivalents/L. Our goal was to investigate the impact of dietary genistein on intestinal development. Piglets (n=8/group) were fed sow milk replacer (MR), MR+1 mg/L of genistein (LG), or MR+14 mg/L of genistein (HG) for 10 d. Formula intake, weight gain, and intestinal length and weight were similar in all groups. Average serum genistein concentration in the HG group was similar to that of soy formula-fed infants. No significant effects of genistein on enterocyte apoptosis, lactase, and sucrase activities or electrophysiologic measures were observed in jejunum or ileum. Jejunal and ileal villus heights were not significantly different, but the percentage of proliferating cell nuclear antigen-positive jejunal crypt cells in the HG was reduced 50% compared with that in MR and LG (p=0.001), indicating decreased proliferation. Enterocyte migration distance in the HG group tended to be 20% less (p=0.1) than LG or MR. Jejunal estrogen receptor beta mRNA expression in HG was half of that in LG (p=0.05), but neither was significantly different from MR. In conclusion, genistein at the level present in soy infant formula is bioactive in the small intestine and results in reduced enterocyte proliferation and migration. The lack of effect of genistein on nutrient transport and enzyme activity suggests that the impact of genistein is greater on proliferating versus differentiated intestinal cells.
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PMID:Genistein inhibits intestinal cell proliferation in piglets. 1558 81