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)

In previous studies we found that in healthy subjects, 5 and 10 g of a partially purified amylase inhibitor delayed and decreased starch digestion and reduced postprandial plasma glucose after a starch meal but produced diarrhea in two of six and four of six subjects, respectively. Thus, we wondered whether lower doses of the inhibitor, when given with a meal that contained protein and fat as well as carbohydrate, would have the same effect on carbohydrate tolerance without causing diarrhea. Eight healthy subjects were randomized to receive 2.0 or 2.9 g of the inhibitor with a 650-calorie meal that contained carbohydrate, fat, and protein. In comparison with a placebo, ingestion of 2.9 g, but not 2.0 g, of the inhibitor significantly reduced postprandial increases in plasma glucose (P less than 0.05), C peptide (P less than 0.03), and gastric inhibitory polypeptide (P less than 0.008). Similarly, 2.9 g of the inhibitor in comparison with 2.0 g was associated with more carbohydrate malabsorption and more breath hydrogen excretion. Because the carbohydrate malabsorption observed with the 2.9-g dose was similar to that with the previously tested 5- and 10-g doses of the inhibitor but diarrhea was less frequent, impurities in the partially purified preparation may, in part, have been responsible for these adverse effects. We conclude that 2.9 g of the amylase inhibitor given with a meal that contains a mixture of nutrients is effective in increasing carbohydrate tolerance without causing diarrhea. Therefore, this dose is appropriate for use in studies to determine whether the inhibitor has a beneficial effect in patients with diabetes mellitus or obesity.
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PMID:Effect of a purified amylase inhibitor on carbohydrate metabolism after a mixed meal in healthy humans. 243 11

Serum pancreatic secretory trypsin inhibitor (PSTI) was measured by radioimmunoassay in 5 patients with malabsorption syndrome. The serum level of PSTI was elevated to 123.8 +/- 25.8 ng/ml (Mean +/- SE) in patients with malabsorption syndrome, which was significantly higher than the 16.6 +/- 0.7 ng/ml level seen in 116 healthy control subjects. Serum PSTI levels in 5 patients with malabsorption syndrome showed inverse correlations with serum levels of cholesterol, cholinesterase and amylase, and not with serum levels of vitamin E, carotene, apoprotein A-IV, albumin, nor with immunoreactive elastase 1, respectively. These results suggest that elevated levels of serum PSTI represent a state of malnutrition due to impaired intestinal absorption.
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PMID:Elevated levels of serum pancreatic secretory trypsin inhibitor (PSTI) in patients with malabsorption syndrome. 243 66

Many previous investigations of available amylase inhibitors have not been able to demonstrate significant carbohydrate malabsorption. This study uses breath hydrogen analysis, a sensitive method for detecting the passage of starch into the colon, to determine if a potent amylase inhibitor is capable of producing carbohydrate malabsorption. Thirteen volunteers underwent three studies, ingesting as a carbohydrate substrate: lactulose 20 g, spaghetti alone, and spaghetti with amylase inhibitor (3.8 g). Samples of breath were collected (at frequent intervals) for 2 h after the lactulose and for 8 h after the spaghetti meal and analyzed for hydrogen concentration. The ingestion of spaghetti alone resulted in significant increases in breath hydrogen concentration at 420-450 min. The mean (+/- SE) hydrogen excretion rate was increased more than 2-fold with the amylase inhibitor, from 0.4 +/- 0.2 to 0.9 +/- 0.3 ml/h (p less than 0.05). Use of the amylase inhibitor in powder form produced a similar increase in the rate of hydrogen excretion to 1.1 +/- 0.4 ml/h. The percentage of carbohydrate malabsorbed was calculated for the spaghetti meal and spaghetti with amylase inhibitor using each individual's observed hydrogen excretion with lactulose. Over the 8-h observation period, 4.7 +/- 1.9% of the spaghetti was malabsorbed and 7.0 +/- 1.4% of the spaghetti with amylase inhibitor was malabsorbed (p less than 0.05). Measurements of the effect of the amylase inhibitor on amylase activity of duodenal juice revealed that the amylase inhibitor at a concentration of more than 5 mg/ml decreased the amylase activity by more than 96%. These results indicate that this potent amylase inhibitor is capable of enhancing malabsorption of wheat starch.
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PMID:Impairment of starch absorption by a potent amylase inhibitor. 244 Feb 98

A partially purified amylase inhibitor given with a single meal causes maldigestion of carbohydrate, increases delivery of carbohydrate to the ileum, and reduces postprandial plasma glucose. To determine the effect of more prolonged administration of the inhibitor on gastrointestinal function and carbohydrate tolerance, we studied 6 non-insulin-dependent diabetics (3 previously treated with oral agents and 3 treated with diet alone) for 3 wk while they ate a weight-maintenance diet. Patients taking oral agents continued them during the first week. During the second week, 4-6 g of the inhibitor was given with each meal. Capillary blood glucose concentration was measured before each meal and 90 min postprandially. On the last day of each week venous blood samples for glucose, hormones, and lactic acid analysis and a quantitative stool culture were obtained. Total carbohydrate absorption was estimated by comparing postprandial breath hydrogen on study days 7, 14, and 21 with breath hydrogen after ingesting 15 g of lactulose on days 0, 15, and 22. There 24-h stools were collected and weighed at the end of each week and analyzed for carbohydrate, lactic acid, short-chain fatty acids, pH, dry matter, amylase, and fat. The inhibitor significantly (p less than 0.05) reduced postprandial plasma glucose, C-peptide, insulin, and gastric inhibitory polypeptide concentrations, significantly increased (p less than 0.05) breath hydrogen excretion, and caused carbohydrate malabsorption. Diarrhea occurred the first day the inhibitor was ingested, but thereafter cessation of diarrhea was associated with changes in the metabolism of carbohydrate by colonic flora. As the amylase inhibitor improves carbohydrate homeostasis and is not associated with continuing diarrhea, it may be a useful adjuvant in the treatment of patients with non-insulin-dependent diabetes mellitus.
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PMID:Gastrointestinal and metabolic effects of amylase inhibition in diabetics. 244 48

The effect of "malabsorption syndrome" on pancreatic function was studied in newly hatched broiler chicks orally inoculated during the first few hours of life with intestinal homogenates from birds with naturally occurring malabsorption syndrome. The control groups were treated with saline. Tissue samples were collected at 0, 2, 4, 6, 9, 13, 17, and 29 days of age from both groups. The BW of inoculated birds decreased significantly relative to that of controls as early as 9 days of age. Pancreatic amylase activity was significantly greater than that in controls by 2 days. Protease activity of inoculated birds increased significantly over that in controls on the 2nd day and decreased significantly on the 6th and 9th days. Reoviruses were detected in the fecal samples of inoculated birds on the 2nd and 3rd days and did not appear in control samples. Reoviruses were also isolated from the pancreatic tissue of two inoculated birds on the 3rd day. Symptoms characteristic of malabsorption syndrome may be elicited by maldigestion; in the present study, this probably resulted from reduced digestive enzyme production of the pancreas. Similarities of changes in plasma triiodothyronine and pancreatic protease levels suggested a possible relationship between thyroid and pancreatic dysfunction in the condition of the malabsorption syndrome.
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PMID:Effect of malabsorption syndrome on pancreatic function in broilers. 248 52

The effect of high fiber diet on fat malabsorption was evaluated in twelve patients with exocrine pancreatic insufficiency secondary to chronic alcoholic pancreatitis. Additionally, the effect of dietary fiber on pancreatic enzymes was examined in vitro, employing different concentrations of cellulose, pectin, and wheat bran incubated with amylase, lipase, and trypsin. Ingestion of a high fiber diet was associated with a small but significant (p less than 0.01) increase in fecal weight and fecal fat excretion. All patients complained of increased abdominal flatulence with high fiber diet, however, no significant increase in frequency of bowel movements was noted. In vitro studies demonstrated reduction in pancreatic enzyme activity by increasing concentration of dietary fiber and its components. These data suggest that steatorrhea may be enhanced with the ingestion of high fiber diet in patients with exocrine pancreatic insufficiency on oral pancreatic enzyme therapy. Increase in fecal fat excretion may, in part, be related to reduction in the activity of pancreatic enzymes by the dietary fiber.
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PMID:Dietary fiber in pancreatic disease: effect of high fiber diet on fat malabsorption in pancreatic insufficiency and in vitro study of the interaction of dietary fiber with pancreatic enzymes. 257 39

The feasibility of using the triolein breath test to demonstrate fat malabsorption was evaluated in a prospective study of patients before and after total gastrectomy and Roux-en-Y reconstruction. Two of 11 patients had subnormal fat absorption before the operation, but 1 and 6 months after the operation 9 of 11 patients had subnormal fat absorption. Peak expiratory 14CO2 (median (range] at the three investigations was 3.9%/h (2.1-5.9%/h), 2.1%/h (1.4-4.5%/h), and 2.0%/h (1.2-6.0%/h), respectively. Patients who underwent a Nissen fundoplication were used as controls. They had normal fat absorption both before and after operation. Serum amylase was not appreciably affected by total gastrectomy and was similar to control values. In contrast, serum albumin decreased 1 month after gastrectomy and recovered after 6 months. In control patients pre- and post-operative albumin concentrations did not differ and were comparable to preoperative albumin values in the total gastrectomy group. The lowered fat absorption may be explained by duodenal bypass with decreased pancreatic stimulation, and it may in part explain the weight loss in patients operated on with total gastrectomy.
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PMID:Fat malabsorption in patients before and after total gastrectomy, studied by the triolein breath test. 273 89

Based upon the clinical finding that a Merck somatostatin-14 (S-14) analog induced steatorrhea in man, we sought to develop animal models to study the effects of S-14 and a series of synthetic analogs on absorption. Rats were trained to eat a diet (preweighed) containing 15% fat. Following the feeding period, the remaining diet was removed and the amount consumed recorded. This food conditioning of the rats was continued until the rats consumed approximately 15 g of the diet per day. Feces were collected and weighed prior to feeding periods. On test days, S-14 or analogs were administered sc to rats immediately prior to feeding. For each compound tested, fat absorption decreased in dose-dependent fashion. For example, S-14 at 0.5 mg/kg did not increase % of dietary fat in feces (% DFF). At 1.0 mg/kg, S-14 increased % DFF from 7.9 to 10.2 (p less than 0.01, pretest day vs test day), and at 10 mg/kg S-14, % DFF increased from 9.1 to 12.8 (p less than 0.001). For each analog, the subcutaneous dose required to decrease fat absorption in rats was several orders of magnitude higher than the intravenous dose required to inhibit insulin and glucagon. Moreover, the threshold for production of statistically significant increases in fecal fat differed among analogs when compared to their endocrine potencies. One analog administered in the model for 14 days was shown to produce consistent fat malabsorption throughout the entire test period; however, this lipid malabsorption was substantially more pronounced on the first three days of the treatment period. When the compound was not administered on day 15, the % DFF significantly decreased. In an attempt to develop a system more suitable for rapid screening, pancreatic secretagogues such as secretin or cholecystokinin, were administered intravenously to anesthetized rats whose duodena had been cannulated and perfused to enable collection of pancreatic secretions. Total amylase, lipase, and protein were determined in single animals in response to a secretagogue, both before and after iv pretreatment by S-14 or an analog. Pancreatic enzyme secretion in response to sequential secretagogue-stimulation was found to be reproducible for up to three injections and behaved in a dose-dependent fashion. In general, secretagogue-induced increases in amylase, lipase, and total protein were comparable. Pretreatment with the S-14 analogs substantially inhibited secretagogue-induced pancreatic exocrine secretion and was dose-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of somatostatin and selected analogs on lipid absorption in animals. 286 42

Protein, fat and carbohydrate absorption in preterm infants fed on human milk or formulae are reviewed. Even in the most premature infants absorption of protein is satisfactory. Nitrogen net absorption is about 85-90% of intake and results slightly lower with human milk than with formulae. The lower apparent digestibility of human milk is probably due to the poorly degraded IgA immunoglobulins and the rapid transit time. Lactose is well tolerated by the preterm infants despite the low lactase activity at birth. Glucose polymers, which have a low osmotic activity and are suitable for increasing carbohydrate intake of formulae, are well absorbed probably for the activity of salivary amylase and brush border glucoamylase, which have been shown to be well developed at birth. Premature infants absorb fat poorly. This malabsorption that increases with the lowering of gestational age is due to low pancreatic lipase activity and to low intraluminal concentration of bile salts. Due to its bile stimulated lipase activity, non-heat-treated human milk used at least in part is an effective method to improve fat absorption in preterm infants. Faecal energy determined using a calorimetric bomb appears to be a simple and an accurate method to predict faecal fat and avoiding expensive and cumbersome analysis.
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PMID:[Absorption of proteins, carbohydrates and fats in the preterm neonate]. 357 19

As aflatoxin causes malabsorption and its toxicity is enhanced by a low protein diet, digestive enzymes formed in the pancreas apparently are influenced by aflatoxin. This hypothesis was investigated in a 2 X 2 factorial experiment. Six groups of 10 egg-type chickens per treatment were analyzed for the absence and presence of aflatoxin (0 and 4 micrograms/g diet) and for normal (12.75%) and low (10.00%) protein in soy-dextrose diets. The specific activities of pancreatic chymotrypsin, amylase, and lipase, but not trypsin, were increased significantly (P less than .01) by aflatoxin. Lowering dietary protein had no effect by itself except to increase amylase activity. Low protein and aflatoxin interacted to lessen but not prevent the effect of aflatoxin on chymotrypsin and amylase. Calculation of total pancreatic activities revealed that aflatoxin increased trypsin, chymotrypsin, amylase, and lipase to 107, 169, 113, and 119%, respectively, of control values on the low protein diet, whereas values were 99, 175, 115, and 115%, respectively, on the normal protein diet. Neither aflatoxin nor low protein altered significantly (P less than .05) the lipid content of fecal material. Thus, aflatoxicosis in egg-type chickens is characterized by a surplus of some digestive enzymes and by normal fecal lipids in contrast to the specific deficiency of amylase and lipase and steatorrhea reported earlier in meat-type chickens. Whereas malabsorption caused by aflatoxin in broilers can be accounted for in part by impaired digestion, this mechanism apparently does not occur in egg-type chickens.
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PMID:Enhanced production of pancreatic digestive enzymes during aflatoxicosis in egg-type chickens. 361 25


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