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)

Dietary aflatoxin at concentrations of 1.25 microgram/g or above caused in broiler chickens a significant (P less than .05) decrease in the specific activities of pancreatic amylase, trypsin, lipase, RNase, and DNase. These enzymes are the primary enzymes of digestion for starches, protein, lipid, and nucleic acids. At concentrations of 2.5 microgram/g or above there was a compensatory pancreatomegaly that resulted in essentially normal total activity for trypsin, RNase, and DNase. Thus, aflatoxicosis was associated with reduced activity levels of enzymes that digest starch and lipid. This digestive deficiency could account for a malabsorption syndrome observed in field outbreaks of aflatoxicosis.
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PMID:Decreased pancreatic digestive enzymes during aflatoxicosis. 617 84

During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc deficiency in human subjects. 636 78

Aflatoxicosis, ochratoxicosis, and T-2 toxicosis were produced by feeding diets containing graded concentration of the appropriate toxin to broiler chicks from hatching unit 3 weeks of age. Aflatoxin, even at levels not growth inhibitory, produced a malabsorption syndrome characterized by steatorrhea, hypocarotenoidemia, and decreased concentrations of bile salts and pancreatic lipase, trypsin, amylase, and RNase. The T-2 toxin at concentrations higher than required to inhibit growth produced a mild malabsorption syndrome characterized by steatorrhea and decreased levels of pancreatic lipase, trypsin, amylase, and RNase. The only suggestion of malabsorption during ochratoxicosis was a severe hypocarotenoidemia. The following observations indicated a lack of correlation between lipid malabsorption and hypocarotenoidemia. The T-2 toxicosis exhibited lipid malabsorption in the absence of hypocarotenoidemia, ochratoxicosis exhibited hypocarotenoidemia in the absence of lipid malabsorption, and aflatoxicosis exhibited both symptoms. These findings imply that carotenoids are physiologically active compounds with specific metabolic processes and are not inert substances swept along with lipids as is commonly assumed from the ability to grow apparently healthy birds free of carotenoids. The current findings also indicate that great specificities exist in mycotoxicoses despite superficial similarities.
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PMID:Comparison of ochratoxin, aflatoxin, and T-2 toxin for their effects on selected parameters related to digestion and evidence for specific metabolism of carotenoids in chickens. 713 18

Cartilage-hair hypoplasia and anauxetic dysplasia are two autosomal recessive skeletal dysplasias characterized by different degrees from metaphyseal to spondylo-meta-epiphyseal dysplasia and variable additional features including predisposition to cancer, anemia, immunodeficiency, and gastrointestinal malabsorption and Hirschsprung's disease. Both are caused by mutations in the untranslated RMRP gene, which forms the RNA subunit of the RNase MRP complex. This complex is involved in the ribosome assembly by cleavage of 5.8S rRNA, cell cycle control by Cyclin B2 mRNA cleavage at the end of mitosis, processing the mitochondrial RNA, and forming a complex with hTERT suggesting a possible involvement in expression regulation by siRNA synthesis. The degree of skeletal dysplasia correlates mainly with the rRNA cleavage activity, whereas significantly diminished mRNA cleavage activity is a prerequisite for immunodeficiency. Thus, the clinical phenotype emerges in most cases of the combined effect on the respective effect on RNase MRP function.
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PMID:The molecular basis of the cartilage-hair hypoplasia-anauxetic dysplasia spectrum. 2139 80