Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied three children with chronic gastrointestinal disease who had been on intravenous hyperalimentation for periods of time ranging from 4 to 23 months. Each child was found to have low plasma and red blood cell glutathione peroxidase activity. This was associated, in the two children tested, with a marked deficiency of serum selenium. Their plasma glutathione peroxidase levels ranged between 4 and 24% of normal and their red blood cell levels ranged between 4 and 14% of normal. The intravenous alimentation was then supplemented with sodium selenite (240 micrograms Se/d). Within 4-5 weeks, the plasma glutathione peroxidase activity returned to normal. Red cell glutathione peroxidase activity remained essentially unchanged for 4-6 weeks, after which it increased over the following 3-4 months. Red cells were separated by density on a continuous Percoll-diatrizoate gradient. In normal individuals, the specific activity of glutathione peroxidase did not differ across the gradient despite a 2.5-fold difference in the specific activity of pyruvate kinase. When studied initially, glutathione peroxidase activity from the deficient patients did not change across the gradient. As the red cell enzyme activity increased with selenium repletion, the highest specific activity was initially found at the top of the gradient (youngest cells). After 3-4 months of supplementation, the specific activity became equal across the gradient. Thus, with selenium repletion, there is a rapid increase in plasma glutathione peroxidase activity, a 4-6 week lag prior to an increase in red cell enzyme activity, and the increase in red cell activity is due to newly synthesized red cells made in the presence of selenium.
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PMID:Selenium repletion and glutathione peroxidase--differential effects on plasma and red blood cell enzyme activity. 392 Aug 95

Selenium status was determined on seven patients receiving long-term intravenous hyperalimentation (IVH) and they were followed monthly for 4 to 17 months. Analysis of the IVH solutions for selenium revealed no detectable amounts. The selenium indices measures were (1) erythrocyte selenium levels, (2) erythrocyte glutathione peroxidase activities (GSH-Px), and (3) plasma selenium levels. In general, the IVH population had significantly lower values (p less than 0.001) for these selenium indices than a healthy population (n = 275). The plasma selenium levels decreased to below the normal range within one to two months after initiation of IVH. The below normal ranges varied by patient: three patients by three months, one patient by nine months, and three patients had low and normal values throughout the study. No consistent correlation of individual patient's erythrocyte GSH-Px activities and erythrocyte selenium levels existed, but a positive correlation (r = 0.51, p less than 0.01) occurred between plasma selenium levels and erythrocyte GSH-Px activities. Thus, erythrocyte GSH-Px activities decrease parallel to decreases in plasma selenium levels but not with changes in erythrocyte selenium levels. These data suggest that some of these IVH patients may be at risk for selenium deficiency and that selenium supplementation of IVH solutions may be required. Furthermore, these data suggest that the measurement of erythrocyte GSH-Px activity or selenium levels in some IVH patients may not be related to available body selenium.
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PMID:Selenium status of seven chronic intravenous hyperalimentation patients. 681 71