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)

Although TPN is used frequently in young infants, little information is available regarding its effect on postnatal development of the gut. The effect of total parenteral nutrition (TPN) and intragastric (IG) alimentation on ontogeny of the small intestine was examined in infant rabbits starting at 10-12 days. Animals were killed at 17-19 days. Body weight, organ weight and weight of segments of proximal, mid and distal small intestine were measured. Intestinal mucosa was scraped, weighed and homogenized for estimation of protein, DNA and disaccharidases. Na+ transport was examined in short-circuited jejunum. Weight gain was similar in controls, sham-treated and TPN animals, but was significantly reduced in IG animals. TPN induced precocious development of sucrase and maltase activity and glucose-stimulated Na+ transport, despite causing a significant decrease in mucosal weight and DNA and pancreatic amylase. IG alimentation also induced precocious development of sucrase, maltase and glucose-stimulated Na+ transport. Thus TPN, despite producing mucosal atrophy and decreased pancreatic exocrine development, stimulates accelerated postnatal maturation of the small intestine.
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PMID:Effects of parenteral and enteral nutrition on postnatal development of the small intestine and pancreas in the rabbit. 310 3

The influence of pancreatic secretions on growth and brush-border enzyme activity, throughout the entire small intestine, was examined in the rat. Pancreatic secretions were excluded from the gut lumen by stapling the pancreatic ducts, without interruption of bile flow. The entire small intestine was studied as four segments; the duodenum and three distal segments of equal length. Weight of intestine and mucosa, and mucosal sucrase, isomaltase, lactase, and alkaline phosphatase activity were measured 10-15 days following pancreatic duct occlusion, or sham-operation. The duodenum of pancreatic duct-occluded animals exhibited significant hypertrophy. In general, specific and total disaccharidase activities were greater in duct-occluded animals than in controls throughout the intestine. The increase was more pronounced in distal than in proximal segments. The sucrase/isomaltase ratio was significantly greater in pancreatic duct-occluded animals than in controls in the two distal segments. Alkaline phosphatase activity was not affected by pancreatic duct occlusion. The greater relative increase of disaccharidase activities and sucrase/isomaltase activity ratios in the distal segments of duct-occluded animals, indicates a more important regulatory role of pancreatic enzymes in the distal small intestine. It is concluded that regulation of intestinal brush-border enzyme activity by pancreatic secretion is selective for enzyme and site as follows: disaccharidases, but not alkaline phosphatase, are regulated; the sucrase subunit of the sucrase/isomaltase complex is most sensitive to regulation, while lactase is least sensitive; and the regulatory effect on disaccharidases is greater in distal than in proximal intestine.
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PMID:Intestinal disaccharidase activity following pancreatic duct occlusion in the rat. 311 40

Gut atrophy develops during prolonged total parenteral nutrition (TPN). TPN solutions do not contain glutamine, an energy substrate of the intestinal tract. This study evaluated the effect of addition of L-glutamine to TPN on gut nitrogen content, histology, and disaccharidase enzyme activity. Five groups of six Fisher 344 rats received rat chow, D5W, TPN (23% calories as lipid), or TPN with 1 or 2% L-glutamine. Animals given TPN received 30 kcal and 0.22 g nitrogen/100 g/day. Metabolic cages allowed nitrogen balance for each group. After 6 days infusion, stomach, small bowel, and colon were assayed for total nitrogen and sucrase, lactase, and maltase activity. Mucosal height and fatty infiltration of the liver were determined from histologic sections. Adding either 1 or 2% L-glutamine resulted in no toxic clinical effects. Glutamine preserved intestinal nitrogen content of the stomach and colon compared to standard TPN and increased nitrogen content of small bowel to greater than that in chow-fed animals. Glutamine maintained mucosal height of the stomach and colon, but was no better than TPN alone in maintenance of small bowel mucosal height. One percent glutamine increased and standard TPN depressed maltase activity compared to chow. Standard TPN and 1% glutamine both stimulated sucrase and lactase activity compared to chow. Addition of 1 or 2% glutamine protected the liver from fatty infiltration seen with standard TPN. These studies would suggest the addition of glutamine might be beneficial during provision of standard total parenteral nutrition.
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PMID:Use of L-glutamine in total parenteral nutrition. 313 88

Glutamine (GLN) is an important fuel and epidermal growth factor (EGF) is a potent mitogen for intestinal mucosa cells. GLN-enriched parenteral nutrition was administered to male Wistar rats, and subcutaneous injections of EGF were given for 3, 6, and 7 days. Control animals were fed a non-GLN-containing solution. Other groups of animals received GLN or EGF alone. Mucosal samples were obtained from the jejunum, ileum, and colon for measurement of weight, DNA, protein, and mucosal thickness. Disaccharidase activity was measured in the jejunum. After 3 days, only animals that received both GLN and EGF had a significant increase in small-bowel mucosal protein and thickness relative to controls. A similar pattern was observed in the colon, where animals that received both agents had a greater mucosal thickness, DNA, and protein content than controls. At 7 days, animals that received EGF or GLN had greater nitrogen retention. In addition, animals that were treated with EGF had elevated sucrase and maltase activity compared with GLN-fed animals at this time. Animals treated with GLN and EGF tended to have increased sucrase activity relative to controls. GLN feeding was associated with increased mucosal DNA and protein contents throughout the intestine for the combined series. EGF increased mucosal DNA and protein in the small intestine but not in the colon. The effect of EGF on the protein content of the small-bowel mucosa was dose dependent. The effects of GLN and EGF on the small bowel and colonic mucosa were additive. These studies suggest that specific nutrients and hormones may be used in combination to decrease the mucosal atrophy that commonly occurs after gut disuse or disease.
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PMID:Combined effects of glutamine and epidermal growth factor on the rat intestine. 313 28

Insulin affects the expression of brush border enzymes by villus cells in vitro and in vivo. Physiological (lactation) and surgical (jejunoileal bypass) models of hyper- and hypoplasia were established so that insulin receptor characteristics could be related to villus histology, expression of sucrase and alkaline phosphatase, and plasma insulin concentrations. In lactating rats, villus height increased up to 55% (p less than 0.005), and fasting plasma insulin increased 71% (p = 0.005), compared with controls. Insulin binding to villus cell membranes, and sucrase and alkaline phosphatase activities were, however, unchanged. In ileum of bypass operated rats, villus height increased 134% (p less than 0.005) while insulin binding fell 68% (p = 0.025). Scatchard analysis revealed that this was largely because of reduction in binding by high affinity receptors. Sucrase and alkaline phosphatase specific activities fell 57% (p = 0.03) and 49% (p = 0.02) respectively, suggesting that ileal villus cells were hypomature. The slightly hypoplastic tissue of selfemptying loops showed normal insulin binding compared to jejunum of sham operated controls. Bypass and sham operated rats had similar fasting plasma insulin concentrations. Reduced insulin binding in markedly hyperplastic gut of bypass operated rats might reflect hypomaturity of villus cells. The reduction in insulin binding, however, might significantly modulate the effect of insulin on small intestinal mucosa and account for the fall in enzyme activity which occurs despite villus hyperplasia.
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PMID:Effects of intestinal adaptation on insulin binding to villus cell membranes. 331 13

Epidermal growth factor (EGF), a major growth factor in human milk, may stimulate growth and development of crucial infant tissues, particularly in conditions where the infant's growth is compromised. Here, we provide evidence of a role for EGF in two such conditions, premature birth and intestinal resection. Compared with women delivering at term, mothers of premature infants produce milk containing higher concentrations of EGF, an effect that is probably maintained throughout lactation. The increased EGF in milk could not be accounted for by a decrease in the volume of milk production or by events surrounding birth, but may instead represent a maternal compensatory mechanism to accelerate growth in pre-term infants. A role for EGF in stimulating adaptive intestinal regrowth following gut resection was identified using weanling rats. Following removal of 50% of the small intestine of weanling rats, inclusion of EGF (20 micrograms/100 g per day) in the diet (S-26 infant formula) significantly accelerated intestinal growth, as determined by wet weight, protein and sucrase activity per unit length. These studies support the concept that administration of EGF could prove beneficial to infants in which crucial, EGF-responsive tissues are poorly developed, e.g. following premature birth or intestinal resection.
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PMID:Is orally-derived epidermal growth factor beneficial following premature birth or intestinal resection? 348 95

We previously have shown that aging alters the expression of several intestinal enzymes during cell migration from the crypt base to the villus tip. The activities of many mucosal enzymes are dramatically altered by starvation and refeeding. We compared the effects of starvation and refeeding on the activities of selected intestinal enzymes in young and aging Fischer 344 rats. Gut mass fell during starvation and rose during refeeding to a similar extent in both groups. Sucrase and maltase specific activities in control aging rats were lower than in young controls and, during starvation, enzyme activities declined at approximately similar rates in both groups. Total duodenal enzyme activities fell by about two-thirds in young animals and by greater than 80% in aged animals. Alkaline phosphatase and adenosine deaminase activities also were lower in aging than young animals. During refeeding, enzyme activities rose more in aging rats than in the young. In fact, the specific activities of sucrase and maltase in aging rats refed for 1 day exceeded the values found in fed aging controls. The adaptive responses of duodenal enzymes exceeded those in the jejunum. In conclusion, the aging intestine responds appropriately to starvation and refeeding. However, the fluctuations in brush-border enzyme activities are much greater in aging than in young rats. Such alterations may be an important influence of aging on gut differentiation and might have an adverse impact upon nutritional maintenance in aging animals.
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PMID:Adaptive changes of intestinal enzymes to nutritional intake in the aging rat. 359 66

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding. 389 54

A simple and reproducible method for cultivation of fetal chicken small intestine is presented. The culture was performed in a defined medium without serum. Duodena were excised from embryos at the 14th day of fetal development and cut in small segments that were maintained in culture until day 16. It could be shown that the morphology of cultured intestine resembles that of noncultured gut of corresponding age as judged by light microscopy. The increase in activity of sucrase and maltase in cultured explants is comparable with that of intestine in ovo, whereas that of alkaline phosphatase is lower than under in vivo conditions. Hormones (thyroxine, dexamethasone) influence the enzymic pattern of fetal intestine in a known manner. Therefore, the method permits maintenance of fetal intestine in tissue culture for 2 days, a period sufficient for investigation of maturation processes of intestinal mucosa.
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PMID:Chicken fetal intestine in tissue culture. 402 13

The effects of an oral neomycin and penicillin regimen on intestinal bacteriology and on morphology and function of the small intestine of mice were investigated. Quantitative and qualitative stool cultures on selective media of the treated animals revealed only growth of yeast organisms. The treated animals developed enlargement of the ceca with fluid contents and watery stools, resembling characteristics of germfree animals. Radioautography with tritiated thymidine revealed an increased epithelial cell migration rate in the mice treated with the antibiotics for 3 to 5 wk. A slight increase in villus height was also noted. The treated male mice showed greater variance than the treated females in epithelial cell migration rates. Histochemical staining reactions showed a decrease in nonspecific esterase and in NADH dehydrogenase activity in the proximal gut of the antibiotic animals. Stains of distal gut and those for acid and alkaline phosphatase, NADPH dehydrogenase, lactic dehydrogenase, and succinic dehydrogenase were similar to the controls. A slight increase in sucrase activity and a slight decrease in lactase activity in the antibiotic animals was observed in contrast to control animals. Germfree mice, however, had greater sucrase and lactase activity. Transport of L-methionine was slightly reduced in the distal segment of the treated animals. Since the direction of these changes is away from the intestinal state observed in germfree animals, they are probably the result of the direct action of the antibiotics on the gut.
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PMID:Effects of neomycin and penicillin administration on mucosal proliferation of the mouse small intestine. With morphological and functional correlations. 438 18


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