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

The neutralization of acid introduced into the duodenum has been found to be less intensive in patients with duodenal ulcer than in controls. The present work studied the possibility that chronic gastric hypersecretion injures the duodenal mucosa and thereby influences the neutralization system. Gastric hypersecretion was provoked for 3 weeks in 3 dogs by a daily injection of a gastrin preparation with prolonged effect. After a subcutaneous injection of this preparation given together with a test meal the acidity of both gastric and duodenal contents was found to increase significantly. After the 3 weeks of gastric hypersecretion the pancreatic bicarbonate response to exogenous secretin was unchanged, while the bicarbonate response to duodenal acidification was decreased from 2.03 mEq/30 min to 1.27 mEq/30 min (p less than 0.05), compatible with an impaired secretin release. Also the concentration of lactase, maltase, sucrase, and alkaline phosphatase in mucosal biopsies from the second part of the duodenum was significantly reduced (p less than 0.001). These results indicate that gastric hypersecretion causes mucosal damage in the duodenum and thereby reduces the release of secretin.
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PMID:Effect of gastric hypersecretion on the canine duodenum. 1 Jun 21

Intestinal DNA, RNA, and protein content were decreased to a greater extent than was body weight when rats were starved for 3 days. Specific lactase and maltase activity increased with progressively longer periods of starvation. Antral and serum gastrin concentration significantly decreased during the 3 days of starvation. Pentagastrin (250 mug/kg 3 times daily) was injected into a group of rats for the duration of a 3-day starvation period and caused a small but significant increase in the relative intestinal RNA and protein content and decreased lactase and maltase specific activities in comparison with the levels of 3-day starved controls. Pentagastrin thus partially reversed some of the starvation-induced changes toward fed levels. Thus, a deficiency in the trophic hormone gastrin may be partially responsible for the disproportionate changes in intestinal tissue during starvation.
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PMID:Relationship between the changes in gastrin levels and intestinal properties in the starved rat. 125 47

This report deals with the effect of feeding inhibitors of pancreatic and brush border enzymes on pancreatic growth and enzyme composition and secretion. Raw soybean flour containing trypsin inhibitors caused pronounced growth of the pancreas which was accompanied by increased enzyme content and increased CCK and gastrin concentration in the plasma. Feeding of an amylase inhibitor to a starch-rich diet induced a marked fall in amylase content and secretion without changing growth parameters of the pancreas, indicating that not starch but glucose is the trigger for the maintenance of amylase content and secretion of the pancreas. The addition of an alpha-glucosidase inhibitor (acarbose) to a sucrose- or maltose-rich semisynthetic diet did not cause significant alteration in pancreatic growth or enzyme composition or secretion. In man pancreatic function was also unaltered by 8 weeks' intake of 3 X 200 mg acarbose.
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PMID:Adaptation of the pancreas during treatment with enzyme inhibitors in rats and man. 240 82

We investigated the effects of pectin, a soluble dietary fiber, on functional and morphological parameters of the small intestine in rats. A control group and a pectin-fed group were given a fiber-free elemental liquid diet and an elemental liquid diet containing 2.5% (w/w) pectin, respectively, for 2 weeks. The ileal mucosal specific activities of maltase, sucrase and alkaline phosphatase increased significantly in the pectin-fed group. Maltose absorption of the ileum, studied in vitro by the method of everted sacs and disaccharide-dependent potential difference, increased significantly in the pectin-fed group. The length of the small intestine as well as the villus height and crypt depth of both the jejunum and the ileum were significantly greater in the pectin-fed group. The crypt cell production rate of the jejunum and the ileum was also significantly greater in the pectin-fed group. Plasma enteroglucagon, but not gastrin, increased significantly in the pectin-fed group. These data suggest that pectin feeding results in hyperplasia of the small-intestinal mucosa and a significant increase in the enzyme activities of the brush border membrane of the ileum.
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PMID:Effect of pectin, a soluble dietary fiber, on functional and morphological parameters of the small intestine in rats. 254 93

Suckling rats were treated every 8 h by intragastric instillation of 16,16-dimethyl prostaglandin E2 (PG) in a dose of 25 micrograms kg-1 (PG25), or 100 micrograms kg-1 (PG100), or saline from postnatal day 7-11. PG increased small intestinal villus length and crypt depth, most markedly in the duodenum, leading to a mucosal height of 543 +/- 24 microns after saline, 670 +/- 26 microns after PG25 and 823 +/- 40 microns after PG100. In the proximal small bowel, PG100 raised the mean activities of sucrase by 439%, maltase by 98%, trehalase by 584%, lactase by 58% and alkaline phosphatase by 76%. In the distal small intestine, only sucrase and trehalase activities were stimulated whereas other enzymes were depressed. PG25 caused similar but less pronounced changes of enzyme activities. Eight hours after both the last PG25 and the last PG100 dose, plasma gastrin and corticosterone levels were decreased while thyroxine remained unchanged. The effect of a single dose of 100 micrograms kg-1 PG or saline was also tested on 5- and 11-day-old rats; they were killed 16 h after PG administration. An increase in villus length occurred along the entire small intestine of rats treated on day 5, and also in the ileum of rats treated on day 11. In the proximal intestine, maltase and trehalase were stimulated after early and late treatment and, in addition, sucrase and lactase after late treatment. Serum corticosterone levels were found to be significantly higher 2-6 h after PG100 than in the controls and then decreased gradually.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of 16,16-dimethyl prostaglandin E2 on small intestinal mucosa in suckling rats. 311 65

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

Although the purified porcine enteroglucagons glicentin and oxyntomodulin inhibit pentagastrin-stimulated gastrin acid secretion when given parenterally to rats, it is not known whether the postprandial rise in endogenous enteroglucagons is capable of exerting a similar effect. We have used the alpha-glucosidase inhibitor acarbose in combination with a sucrose- and starch-rich semisynthetic diet over 8 days to bring about a mean increase of 89 pmol/l in the fasting plasma enteroglucagon concentration in rats, without significantly affecting plasma gastrin concentrations. There was no significant suppression of pentagastrin-stimulated gastric acid secretion in the acarbose-treated rats, suggesting that endogenous enteroglucagons do not act as physiological inhibitors of gastric acid secretion.
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PMID:Pentagastrin-stimulated gastric acid output and plasma enteroglucagon in acarbose-treated rats. 389 16

Frequently, congenital or acquired small intestine (SI) abnormalities in infants lead to inadequate absorption. Gastrin has been suggested as a trophic hormone for SI epithelial cells. We chose to evaluate the effect of gastrin on the function and maturation of developing SI using a rat fetal intestine transplant model. Jejunoileal segments (7-8 cm) obtained from 19 to 20 days gestation fetal rats were implanted subcutaneously in syngeneic adult rats. Two weeks following transplantation the control group (N = 10) was continuously infused with saline and the study group (N = 9) was continuously infused with gastrin-17 (13.5 nM/kg/day) for 14 days. Following the infusion, intestinal maturation and function were evaluated by mucosal DNA concentration, disaccharidase activity, and absorption of [14C]galactose and [14C]glycine. Absorption (microM/cm2 SI) by the control and study groups for galactose was 1.10 +/- 0.18 vs 2.73 +/- 0.25, and for glycine was 1.68 +/- 0.23 vs 2.22 +/- 0.26, respectively. DNA concentration (microgram/mg SI) of the control and study groups was 410 +/- 43 vs 1031 +/- 158, respectively. Lactase and sucrase activity were similar in both groups. Although maltase (microM substrate hydrolyzed/min/g SI) was 13.5 +/- 2.7 for the gastrin group vs 7.9 +/- .9 for the control group, statistical significance was not achieved. Thus, gastrin produced a statistically significant increase in DNA concentration (cell mass) (P less than 0.01). More importantly, to our knowledge, this is the first demonstration that exogenously administered gastrin can increase absorption of carbohydrate (galactose; P less than 0.01) and protein (glycine; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of small intestine function by gastrin. 401 Feb 69

The effect of hydrocortisone (75 mg/kg) on antral, duodenal and pancreatic gastrin concentrations and on intestinal lactase, sucrase, maltase and alkaline phosphatase activities was investigated in suckling rats. Antral and pancreatic gastrin levels in normal 4- to 22-day-old rats were also determined. Hydrocortisone was injected daily to 7- and 10-day-old rats for 6 days. At the end of the experimental period the animals were 12 and 15 days old. Control groups were injected with saline. Hydrocortisone administration caused a profound induction in sucrase activity and markedly stimulated maltase and alkaline phosphatase activities in both age groups. After hydrocortisone administration 12-day-old rats showed a slight (28%) but significant stimulation in lactase activity, whereas in 15-day-old rats the enzyme activity was significantly decreased by 23%, compared to the respective saline control. Gastrin concentration in the antrum increased steadily between 4 and 22 days of age, whereas in the pancreas it decreased sharply from a relatively high level in 4-day-old rats to an essentially undetectable level in 22-day-old rats. Following hydrocortisone administration gastrin concentration in the antrum of 12- and 15-day-old rats was found to be significantly increased by 104 and 47%, respectively, but in the pancreas it decreased by 44 and 57%, when compared with the corresponding saline control. Hydrocortisone caused no apparent change in duodenal gastrin concentration in 12-day-old rats but produced a nonsignificant 35% increment in 15-day-old animals. The observed changes after hydrocortisone treatment are thought to be the result of an early maturation of the gastrointestinal mucosa and pancreas by the steroid.
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PMID:Effect of hydrocortisone on gastrin cell function in various tissues of suckling rats. 641 68

Rats received a daily injection of 2, 6, or 12 mg kg-1 bethanechol for 7 or 14 days. Pancreatic weight and content of protein, amylase, and chymotrypsinogen were increased in a dose and time dependent fashion by bethanechol. After 14 days of treatment with the highest dose, pancreatic weight and total pancreatic DNA content increased to 1.18 times control (P less than 0.05) while protein increased to 1.25, amylase to 1.85, and chymotrypsinogen to 1.72 times control. There was a slight increase in oxyntic gland area weight in bethanechol-treated rats, but content of DNA, protein, and pepsinogen were not changed. Bethanechol had no effect on duodenal weight or content of DNA, protein, or maltase. Acute administration of 12 mg kg-1 bethanechol increased circulating gastrin levels for at least 4 h in unanesthetized rats. We conclude that long-term treatment with a cholinergic agonist produces pancreatic hyperplasia and increases protein and enzyme content. Under the conditions of this study, no effects were seen on oxyntic gland area of stomach or duodenum.
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PMID:Trophic effects of chronic bethanechol on pancreas, stomach, and duodenum in rats. 712 10


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