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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Zinc deficiency was induced in adult male mice by feeding them for 8 weeks on a purified semi-synthetic Zn-deficient diet (ZD) containing 90 g lipid/kg (60 g maize oil plus 30 g cod-liver oil). One group was then fed on a low-lipid Zn-deficient diet (ZDLR) containing 30 g cod-liver oil/kg as the sole lipid source for a further 8 weeks. At the end of the experiment the stomach clearance rate, daily food intake, body-weight gain and [14C]glucose uptake in the intestine were significantly higher in group ZDLR than in mice that continued eating the Zn-deficient lipid-adequate diet ZD, and were comparable to results for a group given a Zn-supplemented diet. These results suggest that the pathogenesis of anorexia, nutrient malabsorption and growth retardation are secondary to lipid malabsorption resulting from Zn deficiency.
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PMID:Influence of low dietary lipid content on anorexia and [14C]glucose uptake in the intestine of zinc-deficient mice. 144 29

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable 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 the population subsisting on cereal proteins mainly. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE, and other chronically debilitating diseases. 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. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. 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. 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. Zinc atoms in some of the enzyme molecules participate in catalysis and also appear to be essential for maintenance of structure of apoenzymes. Zinc also plays a role in stabilization of biomembrane structure and polynucleotide confirmation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and biochemical manifestation zinc deficiency in human subjects. 241 3

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable 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 the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. 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. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. 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. 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and biochemical manifestations of zinc deficiency in human subjects. 258 Aug 77

Zinc deficiency occurs as a genetic disorder, acrodermatitis enteropathica, or as an acquired disorder resulting from inadequate intake or malabsorption of zinc. It is now apparent that human breast milk may not always protect against the development of clinical zinc deficiency in premature and in full-term infants. In the absence of other predisposing factors, low levels of zinc in breast milk may precipitate zinc deficiency in breast-fed infants. This report confirms that breast-fed full-term infants may develop a clinical picture indistinguishable from acrodermatitis enteropathica.
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PMID:Zinc deficiency in two full-term breast-fed infants. 381 64

Zinc deficiency may complicate many gastrointestinal malabsorptive states. Zinc deficiency may manifest itself in a myriad of ways, ranging from skin lesions to immune dysfunction. This paper reports many of the ways in which zinc deficiency may appear in malabsorption syndromes and possible mechanisms for the development of this zinc deficiency.
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PMID:Zinc metabolism in malabsorption syndromes. 388 60

The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal diseases, following uses of certain drugs such as penicillamine for Wilson's disease and diuretics in some cases, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. In pregnancy and during periods of growth the requirement of zinc is increased. The clinical manifestations in severe cases of zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males; it is fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. Its deficiency adversely affects growth in many animal species and humans. Inasmuch as zinc is needed for protein and DNA synthesis and for cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Whether or not zinc is required for the metabolism of somatomedin needs to be investigated in the future. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level; the hypothalamic-pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in cell division, its deficiency may adversely affect testicular size and thus affect its functions. Zinc is required for the functions of several enzymes and whether or not it has an enzymatic role in steroidogenesis is not known at present. Thymopoeitin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. Zinc deficiency affects T-cell functions and chemotaxis adversely. Disorders of cell-mediated immune functions are commonly observed in patients with zinc deficiency. Zinc is beneficial for wound healing in zinc-deficient subjects. In certain zinc-deficient subjects, abnormal taste and abnormal dark adaptation have been noted to reverse with zinc supplementation.
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PMID:Clinical manifestations of zinc deficiency. 389 71

Zinc deficiency has been associated with impared carbohydrate absorption in patients with intestinal disease; however, it is not known whether the carbohydrate malabsorption is caused by the zinc abnormality. Because zinc is needed for protein synthesis, we investigated the effect of zinc deficiency on the total and specific activities of the intestinal glycoprotein disaccharidases. We found that zinc deficiency impairs total body growth and causes marked reductions in intestinal mucosal protein content and disaccharidase activity. However, the protein content and disaccharidase activities were reduced to a similar degree, and both were proportional to the final total body weight. We also found zinc deficiency to have no effect on intestinal villus height or crypt depth. We conclude that zinc deficiency inhibits somatic growth but does not disproportionately affect intestinal mucosal protein content, disaccharidase activity, or intestinal architecture.
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PMID:Does zinc deficiency affect intestinal protein content or disaccharidase activity? 393 98

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

A brief summary of the research carried out on the problem of geophagia is reported in this paper. Geophagia was a common finding among Turkish children and women in villages, associated with severe iron deficiency anemia in addition to zinc depletion. The syndrome characterized by geophagia, iron deficiency anemia, growth retardation, hypogonadism and zinc deficiency has been observed in both sexes in Turkey for several decades. Zinc deficiency has been also shown by our group in this syndrome. The decreased concentrations of zinc in serum, plasma, RBC, hair and urine were measured by atomic absorption spectrophotometer. Oral iron (both inorganic and radioactive iron) and zinc absorption tests were carried out with and without clay and revealed decreased iron and zinc absorption in some cases with prolonged geophagia. Therefore, malabsorption of iron and zinc was considered to be an additional and/or a new finding in the syndrome. Furthermore, Turkish clay most probably inhibits zinc absorption in a way similar to its inhibition of iron absorption. It was worthy of observation that some Turkish patients with this syndrome had a thalassemia-like appearance with similar skull-bone changes. Finally, growth retardation and delayed puberty were shown to be corrected by oral zinc treatment for 6-month terms. Linear growth and sexual maturation were found to be greater in the zinc-treated group than in the controls.
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PMID:Geophagia in Turkey: iron and zinc deficiency, iron and zinc absorption studies and response to treatment with zinc in geophagia cases. 665 8

Protracted diarrhoea in early infancy gives rise to many diagnostic and therapeutic problems. Jejunal biopsy often reveals villous atrophy of varying degrees. Severe reduction of small intestinal absorptive area causes secondary monosaccharide malabsorption, as well as secondary disaccharide deficiency, consequences which are relevant in any attempts at oral feeding. Morphologic, metabolic, endocrinological and microbiological studies have to be undertaken in order to establish a definitive diagnosis in protracted diarrhoea, but these studies often fail to reveal the aetiology of the disease. Immunologic abnormalities like phagocyte dysfunction, thymic atrophy and hypoplasia of B-cell regions in lymph nodes might be secondary events, but some types of immunodeficiency are of primary importance in the development of protracted diarrhoea. Total parenteral nutrition in many cases has to be instituted, with all its implications and hazards: septicaemia is the most dangerous of these. Zinc deficiency and acrodermatitis enteropathica may occur during total parenteral nutrition, and zinc deficiency secondarily contributes to the symptoms of diarrhoea. Parenteral administration of zinc is able to overcome these effects.
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PMID:Protracted diarrhoea: secondary monosaccharide malabsorption and zinc deficiency with cutaneous manifestations during total parenteral nutrition. 677 99


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