Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 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

The authors provide the data obtained during examination of 36 children with celiac disease and 18 children with lactase deficiency. The children's age ranged from 8 months to 15 years. All the children underwent spot biopsy of the gastric and duodenal mucosa followed by immunomorphological PAP-staining of the biopsy specimens and count of the number of gastrin- and somatostatin-producing cells. Gastrin in the blood serum was measured by radioimmunoassay. The children with celiac disease manifested an increase of the number of somatostatin-producing cells in the duodenum and decrease of their number in the pyloric part of the stomach, seen in the acute phase of the disease. The number of gastrin-producing cells remained unchanged. The level of gastrin declined in the acute phase and increased during a remission. The alterations described were found to be related to the atrophic processes in the small intestinal mucosa. In lactase deficiency, no significant alterations were established in the number of pyloric and duodenal endocrine cells or in blood gastrin level.
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PMID:[Disorders of humoral regulation of the digestive organ functions in children with malabsorption syndromes]. 167 86

The effect of chronic administration of hydrocortisone during pregnancy on growth and maturation of the foetal gut and pancreas was investigated. Groups of 10- to 11-day pregnant rats were injected with saline or hydrocortisone (50 mg/kg) once a day for 10 days. The pancreas, antrum, and small intestine of newborns (8-10 h after birth) were analysed for various determinants of growth and maturation. The small-intestinal weight and DNA, RNA, and protein were significantly higher in newborns from hydrocortisone-treated animals than those of saline-treated controls. Hydrocortisone treatment resulted in an induction of sucrase and significantly stimulated total lactase activity. After the steroid treatment during pregnancy, the weight of the pancreas and its DNA content in newborns were also significantly elevated when compared with those from saline-treated controls. However, neither pancreatic RNA nor protein content differed significantly between the groups. Antral gastrin content in newborns from hydrocortisone-treated mothers was significantly higher than that from saline-treated controls. Pancreatic gastrin content in newborns was slightly but not significantly reduced after the steroid administration to mothers. It is concluded that glucocorticoids induce growth and maturation of foetal gut and pancreas.
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PMID:Influence of glucocorticoids on prenatal development of the gut and pancreas in rats. 258 7

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

Rats were kept undernourished from birth to 24 days of age. At 17 days of age, the undernourished animals were divided into two groups and then injected with either saline or epidermal growth factor (EGF; 20 micrograms/kg) once a day for 7 days. They were killed 12-14 h after the last injection at which time the animals were 24 days old. During the experimental period the undernourished animals were prevented from weaning. A well-nourished group (weaned) which was injected with saline from 17 to 24 days of age, was also included. Undernutrition by itself significantly decreased body weight and the weight of the oxyntic gland area, antrum, and small intestine. This was also accompanied by a parallel reduction in DNA, RNA, and protein content in the oxyntic gland and small intestine. However, administration of EGF to undernourished rats resulted in a partial reversal of the situation. In undernourished rats, EGF caused significant enhancements in body weight as well as the weight of the gastrointestinal tissues and their protein and nucleic acid content when compared with the saline-treated undernourished controls. Furthermore, the magnitude of stimulation was found to be greater in the oxyntic gland than in the small intestine following EGF administration. The antral or serum gastrin levels were not affected by EGF. In both saline- and EGF-treated undernourished rats, lactase, sucrase, and alkaline phosphatase activities (expressed as total or specific activity) were found to be significantly higher than in the well-nourished animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postnatal undernutrition: effect of epidermal growth factor on growth and function of the gastrointestinal tract in rats. 620 84

The role of gastrin and cholecystokinin (CCK) in postnatal development of the small intestine was examined in infant rabbits. Experimental animals received daily intraperitoneal injections of pentagastrin, 500 micrograms/kg, or CCK-octapeptide, 40 micrograms/kg, starting on day 3 of life. The animals were sacrificed at age 17-18 days. Weight and histologic sections of pancreas, stomach, duodenum, proximal jejunum, and ileum were obtained and mucosal lactase and sucrase activities determined in the intestinal segments. No differences were seen in any of the parameters assessed in pentagastrin-treated animals compared to saline-injected littermate controls. Body weight, weight and morphology of pancreas, stomach and intestinal segments, and enzyme activities did not differ significantly. Na+ transport in proximal jejunum under short-circuited conditions was not altered by pentagastrin. CCK-octapeptide also had no effect on weight or morphology of pancreas, stomach, and duodenum, but did lead to a significant increase in weight of proximal jejunum and ileum. Mucosal enzyme activities and morphometric measurements of villus height and mucosal thickness, however, did not differ significantly between CCK-octapeptide-treated animals and saline-injected littermate controls. The increase in weight of jejunal and ileal segments was reflected by an increase in thickness of the muscle layer. The findings indicate that neither gastrin nor CCK plays a role in the ontogenic development of the small intestine.
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PMID:Role of gastrin and cholecystokinin in the ontogenic development of the gastrointestinal tract. 632 Sep 13

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

To evaluate whether the small bowel can be distracted by mechanical stress in analogy to limb lengthening by osteodistraction, a gut-lengthening apparatus was designed. This distractor was placed at the antimesenterical side of a defined jejunum segment in rabbits. Distraction was performed by 1 mm lengthening of the distractor once daily using extracorporal screws. An effective gut lengthening was achieved of 9.9 +/- 0.5 mm (approximately 100%) within 3 weeks. Treated animals gained weight and remained in good general condition. Fasting plasma levels of cholecystokinin, neurotensin, glucagon-like peptide-1, gastric inhibitory polypeptide, and insulin remained unaffected. Postoperative factor XIII levels were significantly diminished and gastrin was elevated during gut distraction. DNA and protein concentrations in the mucosa of the distracted gut segments corresponded to controls. Mucosal lactase and saccharase activities were reduced. In the distracted bowel segments total tunica muscularis thickness was more than doubled due to muscle cell hypertrophy. In distracted segments villous width was increased. Detection of proliferating mucosal crypt cells utilizing BrdUrd labeling revealed no effects. In conclusion, small gut lengthening by mechanical distraction is possible without major changes in gut morphology. This technique may hint a novel experimental approach for the treatment of short bowel syndrome.
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PMID:Small bowel lengthening by mechanical distraction. 924 19

At birth, the mammalian gastrointestinal tract (GIT) must be able to support a shift from mainly parenteral nutrition in the fetus (via the placenta) to enteral nutrition in the neonate. In the perinatal period the GIT therefore undergoes enhanced growth as well as morphological and functional differentiation, and this maturational programme is influenced by a complex interplay of local, systemic and luminal factors. This review shows how systemic and luminal factors may influence GIT development in the perinatal period of the pig and sheep, two long-gestation species. Adrenocortical hormones play a pivotal role in the prepartum maturation of the GIT in addition to their better known effects on the development of many other tissues and body systems. More particularly, in the fetal pig and sheep, the prenatal development of gastric acid and gastrin secretion, and of GIT hydrolase activities (chymosin, pepsin, amylase, lactase, aminopeptidases) is influenced by cortisol. Additionally, glucocorticoids exert effects throughout the GIT by influencing morphological, cytological, and functional differentiation. Since the GIT epithelial cells comprise a renewing cell population there are also changes in cell kinetics. In addition to systemic factors, the presence of growth factors, hormones and nutrients from swallowed amniotic fluid (fetus) and colostrum (neonate) may influence GIT development. In utero, fetal fluid ingestion has been shown to modulate tissue growth, macromolecule and immunoglobulin transport, enterocyte differentiation, cell turnover and activity of brush-border hydrolases. These effects may be mediated via regulatory peptides (e.g. insulin-like growth factor I, gastrin-releasing peptides, insulin, epidermal growth factor, gastrin). A physiological role of luminally derived growth factors is supported by a number of unique structural and functional adaptations of the GIT in the fetus and neonate (low luminal proteolysis, intestinal macromolecule transport). Thus, in the pig and sheep, both systemic and luminal factors appear to play critical roles in GIT development in the perinatal period.
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PMID:Systemic and luminal influences on the perinatal development of the gut. 935 1


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