Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment was conducted to examine the effect of pathogenic Escherichia coli inoculated into the yolk sac of day-old turkeys. Escherichia coli was isolated from the yolk sac of stunted poults and inoculated directly into the yolk sac of day-old birds. Poults were administered either .1 ml of uninoculated sterile Todd-Hewitt broth or .1 ml of a 10(-3) or 10(-2) dilution of a 24-hr E. coli culture containing 3.4 X 10(8) viable bacteria/ml. In addition, poults were fed either 28 or 22% protein diets from 0 to 21 days of age to form a 3 X 2 factorial arrangement. Body weight gain and feed consumption were measured weekly, and dry matter and protein retention and nitrogen-corrected metabolizable energy were measured from 7 to 10 and 17 to 20 days postinoculation. Intestinal mucosal dipeptidase and maltase activities were determined at 21 days of age. Average mortality by 7 days of age was increased from 1 to 36% from the E. coli inoculation of the yolk sac. Escherichia coli significantly depressed body weight gain and feed consumption 27 and 30, 13 and 16, and 6 and 8%, respectively, during the first, second, and third weeks of the experiment but failed to affect feed efficiency. Feeding a 28% protein diet alleviated the depression in feed consumption and body weight gain to some extent compared with a substantial depression at 22% protein. Nitrogen content and gross energy of the excreta were increased by both dilutions of E. coli for the 7 to 10-day period; this was indicative of a malabsorption of nutrients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary protein and yolk sac inoculation with Escherichia coli in young turkeys. 389 12

Acarbose is an alpha-glucosidase inhibitor which reversibly and competitively inhibits the digestion of oligo- and disaccharides at the brush border of the small intestine. This study evaluates the preventive and therapeutic properties of acarbose in the treatment of obesity. Dose-response experiments were performed during repeated sucrose loads in man in order to investigate the effects of acarbose on plasma insulin and blood glucose levels. After titration of efficient doses, a long-term tolerance test of acarbose was undertaken in a small pilot study. Finally, the relapse preventing effect of acarbose was tested during double-blind cross-over conditions in 24 weight reduced obese women. In growing Sprague-Dawley rats, the effects of acarbose on body weight, lipid depots and adipose tissue cellularity were tested during pair-feeding and ad libitum conditions. Such effects were also studied in adult ad libitum-fed rats. Blood glucose, plasma insulin, body fat, depot lipids as well as fat cell weight and number were determined with established techniques. During a sucrose load, acarbose reduced insulin in a dose-dependent fashion. Glucose was also reduced, but not dose-dependently and only to a moderate extent. During a 200 g sucrose load, 400 mg of acarbose did not necessarily result in a maximal reduction of the insulin response while the glucose response was maximally inhibited after 100 mg. Acarbose reduced the relapse rate after weight reduction. No serious side effects were observed. Flatulence and meteorism occurred frequently. In growing rats, acarbose retarded the development of body weight and of lipid depots not only during pair-feeding conditions but also in ad libitum-fed animals eating considerably more than their controls. The spontaneous food consumption was increased by acarbose also in adult rats but in these animals neither body weight nor lipid depots were significantly reduced by acarbose. It is concluded that acarbose induces a carbohydrate malabsorption. Insulin levels are reduced not only via a decreased glycemic stimulus but also by interference with other insulin releasing mechanism(s). Acarbose is the first drug ever tested with long-term relapse reducing effects after weight reduction. Animal experiments suggest that acarbose may be of value in the prevention of obesity, particularly since the drug retards lipid accumulation also during ad libitum-feeding.
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PMID:alpha-Glucosidase inhibition in obesity. 391 27

The definition of "insufficient" small bowel lactase activity varies greatly among authors. The present study is aimed at redefining lactase insufficiency by comparing intestinal lactase activity and results of the lactose breath hydrogen test. Primary "insufficient" lactase activity was considered to be present when a child with a normal small bowel histology showed lactose malabsorption as measured by the lactose breath hydrogen test. The lactase activity of 22 "normal" children ranged from 0.77 to 4.57 U/g wet weight, while five children showed primary lactase insufficiency as defined above. Small bowel lactase activity in the latter patients was less than 0.74 U/g wet weight. Sucrase and maltase activities were similar in both groups of patients. We conclude that children with a normal small bowel histology should be considered to have primary lactase insufficiency when small bowel lactase activity is below 0.75 U/g wet weight.
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PMID:Lactase insufficiency revisited. 393 58

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemic excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose [(1-14C]glucose and a simultaneous intravenous infusion of [3-3H]glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemic excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.
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PMID:The effects of an alpha-glucoside hydrolase inhibitor on glycemia and the absorption of sucrose in man determined using a tracer method. 636 57

In 30 children presenting with complaints characteristic of malabsorption in whom congenital enzyme deficiency could be excluded, determination of the enzymes lactase, saccharase and maltase was performed in the tissue sample obtained by jejunal biopsy; histology was also carried out in all cases. In 23 cases the diagnosis of coeliac disease could subsequently be confirmed, in the other 7 cases the diagnosis could neither be rejected nor established with certainty. All three enzymes had a decreased activity in cases displaying subtotal or total villous atrophy, the most sensitive among them being lactase: in 69% of cases no lactase activity could be shown while saccharase and maltase were absent in 29 respectively 4% of the cases. No close correlation exists between the light-microscopic findings and the activity of enzymes since total absence of enzyme activity may be associated with only moderate villous atrophy. Lack of disaccharidase activity in the upper section of the small bowel does not necessarily mean disaccharide malabsorption exhibiting clinical symptoms, it only indicates a reduced capacity of disaccharide splitting. It has been concluded that routine determination of disaccharidase activities is not justified within the diagnostic procedure of coeliac disease.
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PMID:Disaccharidases in coeliac disease. 641 72

Administration of the alpha-glucosidase inhibitor, acarbose (BAY g 5421), to rats together with a sucrose load results in a marked retardation of sucrose digestion. The carbohydrate content of the small intestine is dose dependently increased; the time needed for the absorption is doubled. In the large intestine significant amounts of carbohydrate can be found only after administration of high doses of acarbose (2-4 mg/kg p.o.). In oral sucrose and maltose loading tests the blood glucose increase is dose dependently reduced by acarbose (ED50, 1 or 12 mg/kg, respectively). In perfused jejunal loops of rats, acarbose inhibits the absorption of sucrose (4 g/l) and maltose (1 and 2 g/l), the IC50 values being 3.2, 36, and 57 micrograms/ml, respectively. The data indicate that acarbose effectively inhibits sucrose digestion. It is 10-20 times less effective with maltose as a substrate. Slight malabsorption is induced by acarbose only in doses higher than the ED50.
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PMID:Inhibition of disaccharide digestion in rat intestine by the alpha-glucosidase inhibitor acarbose (BAY g 5421). 675 13

There are at least 20 rare autosomal recessive disorders that are excessively common in Finland of which congenital lactase deficiency is one. During the last 17 years we have found 16 cases. In each case the mother noted watery diarrhoea, generally after the first feed of breast milk, and at the latest, by age 10 days. The lactose malabsorption was verified at a mean age of 36 (range 3-90) days, by which time the infants were dehydrated and 15 of them weighed less than at birth (mean weight for age was -2.8 SDs). On a lactose-free elimination diet (a group of 6 on Nutramigen and a group of 10 on soy-based formula) the children caught up in growth. One infant in each group showed allergic symptoms. While the infants were being breast fed their faeces contained 20 to 80 g/l lactose. In 24 peroral lactose tolerance tests, the greatest rise in blood glucose concentration was 0.8 mmol/l. Only 2 patients showed abnormal absorption when tested within a week of lactose elimination, and in each absorption tests became normal during the elimination period. Slight to partial villous atrophy of the jejunum was present in 4 early specimens, but in later ones the mean villous height was normal. The mean height of the epithelial cells was reduced and there were fewer intraepithelial lymphocytes in patients. The lactase activities in jejunal biopsy specimens were lower than in most patients with acquired lactase deficiency, with some overlap. The maltase and sucrase activities were normal.
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PMID:Congenital lactase deficiency. A clinical study on 16 patients. 684 26

Acarbose (Bay g 5421) is a powerful alpha-glucoside hydrolase inhibitor of potential value in the treatment of diabetes and hypoglycemic dumping syndrome after gastric surgery. The extent of its use may be limited by symptoms produced by carbohydrate malabsorption. To minimize these, the action of low doses of acarbose on 24-h blood glucose profiles and hydrogen evolution have been studied on four ambulant volunteers on control diets, after exclusion of sucrose and also after addition of guar in an attempt to enhance the therapeutic effect. Replacement of dietary sucrose by starch abolished significant hydrogen evolution in the morning after low doses of acarbose but did not reduce its effectiveness in decreasing the mean three-meal blood glucose area by 41% (P less than 0.002). Addition of hydrated guar to this diet reduced the mean three-meal glucose area after acarbose further by 72% (P less than 0.001) but increased hydrogen evolution. The results suggest that acarbose will be both effective and acceptable given at low dose when the dietary carbohydrate is starch.
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PMID:Effect of acarbose on the 24-hour blood glucose profile and pattern of carbohydrate absorption. 692 27

Fifty-gram carbohydrate tolerance tests were performed on healthy volunteers to test the activity and specificity of an alpha-glucoside hydrolase inhibitor, acarbose (BAY g 5421). Two hundred milligrams acarbose reduced the area under the blood glucose response curve by 89% (P less than 0.001) after sucrose by 80% (P less than 0.002) after starch, by 19% (N.S.) after maltose, with no effect on glucose. Breath hydrogen measurements indicated an almost complete malabsorption of the sucrose. At 50 mg acarbose, some reduction in blood glucose and insulin response to sucrose was still seen, but no significant hydrogen production. It is suggested that at lower doses, acarbose may prolong the time course over which carbohydrate is absorbed as does dietary fiber; as with fiber, it may be a useful adjunct to diabetic therapy.
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PMID:Scope and specificity of acarbose in slowing carbohydrate absorption in man. 702 48

The influence of metronidazole on the breath hydrogen response and symptoms of sucrose malabsorption was investigated in a double-blind, randomized and controlled study. Carbohydrate malabsorption was induced by the competitive alpha-glucosidase inhibitor, acarbose. Metronidazole reduced flatulence and the breath hydrogen response during sucrose malabsorption without a change in intestinal carbohydrate absorption, as indicated by serum levels of gastric inhibitory polypeptide, serum insulin and blood glucose. The effect of metronidazole suggests that anaerobic bacteria mediate both signs and symptoms of the colonic response to sucrose malabsorption. In contrast to previous reports on lactose malabsorption, it was not possible to quantify sucrose malabsorption by comparing the breath hydrogen response to sucrose malabsorption with the H2 response to a lactulose load.
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PMID:Influence of metronidazole on the breath hydrogen response and symptoms in acarbose-induced malabsorption of sucrose. 716 May 49


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