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)

Megalocytic anemia of alcoholics is due to the deficiency of folic acid: the proof is the serum hypofolemia. The mechanism is complex and due to : a dietary deficiency; a malabsorption; an insufficiency of conversion of polyglutamate to monoglutamate; a liver deficiency; a specific effect of alcohol on the folate absorption. Alcohol has a toxic effect on the marrow and inhibits the folic acid.
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PMID:[Megalocytic anemia of alcoholics and folic acid (author's transl)]. 626 99

Ethanol has important effects on the alimentary tract. Nearly every study in the literature documents some aberration of absorption or metabolism of multiple vital nutrients. Malnutrition related to both poor dietary intake and malabsorption plays an important role in the clinical problems of chronic alcoholics. From a clinical viewpoint, the assessment of nutritional status by standard techniques, including serum assays for vitamins and trace elements may add to the ability to treat the alcoholic for potentially detrimental disorders. Malabsorption of ingested nutrients is common, despite the lack of salient physical findings. Therefore, parenteral administration of nutrients may be advisable, pending the reversal of the exocrine and intestinal mucosal defect. Increasing awareness of such deficiencies may lead to their earlier recognition, appropriate therapy, and prevention of further complications.
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PMID:The effect of alcohol on the human alimentary tract: a review. 635 Apr 22

There is evidence for both humans and rats that malnutrition frequently occurs when ethanol is chronically ingested. Small bowel 14C-labelled glucose absorption was measured with an ex vivo system in which the small bowel of the rat was surgically removed and then arterially perfused with an artificial medium. Glucose absorption for a control group of seven rats was 248 +/- 8 microM/min/gm dry weight of small bowel (mean +/- SEM). This was significantly greater than the value 112 +/- 12 microM/min/gm dry weight (P less than 0.005) for a group of five rats in which a competitive inhibitor of glucose absorption, phlorizin (0.2 mM), was added to the bowel lumen. In the presence of 3% ethanol within the gut lumen of five rats, glucose absorption was also reduced (to 131 +/- 12 microM/min/gm dry weight) compared to absorption in the control group (P less than 0.005). The calculated amount of glucose absorbed was corrected for metabolism to lactate and carbon dioxide. We conclude that both phlorizin and ethanol inhibit glucose absorption in the isolated and perfused small bowel of rats and that probably at least part of the malnutrition in ethanol-fed rats is due to glucose malabsorption.
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PMID:Ethanol inhibition of glucose absorption in isolated, perfused small bowel of rats. 641 May 24

The effect of chronic alcohol consumption on vitamin A metabolism was investigated in male rats. Liquid diets containing five times the NRC requirement for vitamin A and varied levels of ethanol were fed. The vitamin A content of the liver was decreased in rats receiving alcohol. Liver lipids were only slightly elevated in alcohol-fed rats. Hepatic vitamin A storage was also decreased in rats fed 30% calories as alcohol and beta-carotene or vitamin A at the NRC requirement level, but not in rats fed one-sixth the NRC requirement as vitamin A. The activities of alcohol dehydrogenase, NADPH cytochrome c reductase, and retinol dehydrogenase were not altered in hepatic or testicular tissue by the vitamin A or alcohol content of the diet. When an intragastric dose of [3H]retinyl acetate or [14C]beta-carotene was administered, fecal excretion of radioactivity was lower than controls in rats receiving 30% ethanol in the diet for a total of 4 weeks, for 1 week following 7 weeks of control diet consumption, and after an acute dose of ethanol. Recovery of the 3H label was greater in the testes of rats chronically consuming ethanol. When a solution containing [3H]retinyl acetate or [3H]beta-carotene with or without ethanol was injected into intestinal segments, no alterations in absorption of retinyl acetate or beta-carotene due to ethanol occurred. It is concluded that alcohol consumption results in decreased hepatic vitamin A storage, which is not due to the malabsorption of either retinyl acetate or beta-carotene, or to altered activities of several enzymes involved in ethanol and vitamin A metabolism.
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PMID:Effect of chronic alcohol consumption and moderate fat diet on vitamin A status in rats fed either vitamin a or beta-carotene. 668 29

The use of a few microcuries of 14C labelled molecules with very short biological half-life for breath-tests gives no more body irradiation than 10 minutes' exposure to the sun. Yet it provides the gastroenterologist with accurate information. Detection and identification of fat malabsorption are easy when 3 labelled lipids are used. Glycine 1 14C cholate administered orally offers a simple, rapid and effective screening technique for the detection of increased bile salt deconjugation and may provide a valuable diagnostic supplement in the study of steatorrhea after ileal resection, bypass or bacterial overgrowth. The clearance of labelled aminopyrine can be decreased in hepatocellular dysfunction or increased in some alcoholic patients or in patients receiving phenobarbitone. Tracer doses of labelled ethanol were used to study the metabolism of ethanol by the liver in alcoholic patients. Chronic ingestion of alcohol stimulates the activity of microsomal drug-metabolising enzymes in both non-cirrhotic and cirrhotic patients; this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction. The CO2-labelled breath-tests are non-invasive, effective and inexpensive. The forthcoming replacement of 14C by non-radioactive 13C or briefly radioactive 11C will render these tests even more attractive.
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PMID:[Labelled CO2 breath-tests in gastroenterology (author's transl)]. 679

The effect of chronic ethanol ingestion on the ability of the small intestine to absorb zinc was examined in male Sprague-Dawley rats. Six rats were fed the Lieber-Decarli liquid rat diet for 1 month during which 36% of their total calories were provided as ethanol, while their pair fed controls received these calories as carbohydrate. Zinc absorption was then examined simultaneously in duodenal and ileal segments by in vivo perfusion. Net absorption of zinc in the ileum was reduced by 16% following chronic ethanol feeding. Duodenal absorption of zinc was significantly less than in the ileum and was unaffected by chronic ethanol ingestion. These results demonstrate that chronic ethanol ingestion significantly impairs net zinc absorption in the ileum of the rat, the most active area of zinc uptake as measured by in vivo perfusion, and suggest that malabsorption of zinc may contribute to the zinc deficiency seen following chronic ethanol ingestion.
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PMID:Effect of chronic ethanol ingestion on zinc absorption in rat small intestine. 686 90

A 28 year old woman with Hashimoto's disease was treated with desiccated thyroid and triiodothyronine (T3). She improved steadily during the first 2 to 3 months and thyroidal function tests turned to normal. Then, in spite of continuing treatment, her serum T4 level decreased gradually and she became fatigued. A serum T3 radioimmunoassay manifested an interference pattern suggested anti-T3 antibody in her serum. Ethanol-extracted serum T3 and T4 levels were low in spite of ingestion of desiccated thyroid or synthetic T3 and T4, suggesting intestinal malabsorption of T3 and T4. Antibodies against T3 and T4 were identified in her serum; affinity constants were 1.16 X 10(10) and 8.73 X 10(8) l/mol respectively. After treatment with synthetic T3 and/or T4 for 20 months, the titer of anti-T3 and anti-T4 antibodies decreased, and impaired intestinal absorption of thyroid hormone improved. Then, after desiccated thyroid treatment was reinstituted, the anti-T3 antibody titer again increased and intestinal absorption of thyroid hormone decreased. These results suggest the oral immunization against thyroid hormones. There was associated impairment in intestinal absorption of thyroid hormone presumably secondary to the anti-T3 and anti-T4 antibodies.
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PMID:[Impaired intestinal absorption of thyroid hormone in a case of Hashimoto's disease with anti-T3 and anti-T4 antibody]. 689 78

A toxic effect of alcohol is the principal cause of the development of liver disease in alcoholism. Fatty infiltration of the liver is a consequence of ethanol metabolism due mainly to an increased synthesis and decreased degradation of fatty acids. Mechanisms that have been suggested for ethanol-induced hepatocellular necrosis include centrolobular hypoxia due to an increased oxygen requirement and intracellular accumulation of protein, fat, and water which results in increased cell size. Hepatocellular necrosis, however, may not be a necessary stage in the development of cirrhosis. Chronic ethanol administration increases hepatic collagen deposition, and acute and chronic ethanol administration inhibit liver cell regeneration. Increased humoral and cellular immunological activity to liver tissue and its components may contribute to the persistence of liver disease in the alcoholic. However, only a small proportion of alcoholics and baboons fed alcohol develop cirrhosis, suggesting that other factors, either genetic, environmental, or nutritional, play a role. Malnutrition is common in alcoholics. Liver disease is more common in some malnourished populations, and has been produced by nutrient deficiencies. Decreased dietary intake, as well as malabsorption and alterations in the metabolism of nutrients, are causes of nutrient deficiencies in alcoholism. Some of the effects of alcohol on the liver may be mediated by its actions on nutrient absorption and metabolism.
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PMID:Alcoholic liver disease: roles of alcohol and malnutrition. 700 89

Vitamin A and zinc metabolism are affected both by ethanol and by hepatic cirrhosis. Ethanol causes abnormal dark adaptation by acting as a competitive inhibitor with retinol for alcohol dehydrogenase in the eye. In animals oral ethanol intake results in increased losses of zinc by the urinary and fecal routes. Vitamin A malnutrition in cirrhotics may be caused by poor diet, malabsorption, decreased hepatic vitamin A uptake, and decreased hepatic storage capacity for vitamin A. In some cirrhotic patients zinc deficiency and or protein deficiency may limit the ability to respond to vitamin A. Combined vitamin A and zinc deficiencies are common in cirrhotics and either may result in abnormal dark adaptation or impaired taste and smell. The interaction of these two micro-nutrients must be kept in mind by the clinician caring for alcoholic or alcoholic cirrhotic patients.
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PMID:Vitamin A and zinc metabolism in alcoholism. 700 92

The intestinal absorption of labeled folic acid ([3H]pteroylmonoglutamate) was determined from urinary and fecal recoveries of tritium in pairs of monkeys fed control liquid diets or diets containing 50% of energy as ethanol for a 24-mo period. Weight gain, fecal fat excretion, nitrogen balance, D-xylose absorption, serum folate levels, jejunal histology, and intestinal enzyme activities were similar in each group. Liver biopsies obtained after 12 and 24 mo of feeding demonstrated steatosis and megamitochondria in the ethanol-fed group, with decreased hepatic levels of folate at 24 mo. Intestinal malabsorption of labeled folic acid in the ethanol-fed monkeys was indicated by decreased urinary recovery of tritium but increased fecal recovery of tritium after intragastric administration of [3H]pteroylmonoglutamate. These studies suggest that folic acid malabsorption follows the chronic administration of ethanol together with a nutritious diet.
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PMID:Intestinal absorption of [3H]folic acid in the chronic alcoholic monkey. 719 63


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