Changes in plasma zinc content after exercise in men fed a low-zinc diet

1984 ◽  
Vol 247 (1) ◽  
pp. E88-E93 ◽  
Author(s):  
H. C. Lukaski ◽  
W. W. Bolonchuk ◽  
L. M. Klevay ◽  
D. B. Milne ◽  
H. H. Sandstead

For 30 days five healthy men aged 23-57 yr consumed a diet adequate in zinc (8.6 mg/day); they ate a low-zinc diet (3.6 mg/day) for the next 120 days and then received a zinc-supplemented (33.6 mg/day) diet for 30 days. Copper intake was constant at 1.8 mg/day. Aerobic capacity was determined periodically during each diet period. Relative zinc balance (% of control) declined during depletion (r = -0.28, P less than 0.009). Pre- and postexercise zinc concentrations decreased when dietary zinc was restricted (r = -0.61, P less than 0.0001 and r = -0.78, P less than 0.0001) and increased with supplementation (r = 0.61, P less than 0.008 and r = 0.76, P less than 0.0003, respectively). Both plasma zinc and hematocrit increased (P less than 0.01) after maximal exercise. To minimize the effect of hemoconcentration during exercise, the van Beaumont quotient (J. Appl. Physiol. 34: 102-106, 1973) was calculated using pre- and postexercise hematocrit and plasma zinc. The initial quotient of 1.8 +/- 1.8% (mean +/- SE) declined (P less than 0.05) to -7.4 +/- 2.3% during depletion. With zinc repletion, the quotient increased to 6.9 +/- 3.6%, which was greater (P less than 0.05) than the quotient in depletion but similar to the initial quotient. The quotient was a strong predictor (r = 0.71, P less than 0.0005) of the change in relative zinc balance during zinc depletion. In contrast, no changes were found in plasma copper content. These data suggest that zinc mobilization from tissues is impaired during zinc depletion, and they validate the use of the van Beaumont quotient as an index of change in body zinc stores.

2015 ◽  
Vol 68 (9) ◽  
pp. 723-725 ◽  
Author(s):  
Andrew Duncan ◽  
Calum Yacoubian ◽  
Neil Watson ◽  
Ian Morrison

AimsIn high doses zinc may cause copper deficiency, a diagnosis that is often missed resulting in anaemia, neutropenia and irreversible neurological symptoms. The aim of this study was to assess if zinc deficiency is erroneously diagnosed by misinterpretation of plasma zinc concentrations and whether copper deficiency is induced in patients prescribed zinc.MethodsCasenotes of 70 patients prescribed zinc were scrutinised. Plasma concentrations of zinc, copper, C reactive protein and albumin were recorded from the laboratory database.Results62% of patients were prescribed zinc at doses sufficient to cause copper deficiency. In 48% of the patients, plasma zinc concentrations were low as a probable result of hypoalbuminaemia or the systemic inflammatory response rather than deficiency. Awareness of copper deficiency was lacking; it was only documented as a possible side effect in one patient and plasma copper was measured in only two patients prescribed zinc. 9% of patients developed unexplained anaemia and 7% developed neurological symptoms typical of copper deficiency.ConclusionsZinc deficiency is frequently misdiagnosed on the basis of low plasma zinc concentrations. The potential risk of copper deficiency developing in patients prescribed high doses of zinc is apparently infrequently considered. It is probable that a significant minority of patients prescribed with high doses of zinc develop iatrogenic copper deficiency.


1976 ◽  
Vol 231 (1) ◽  
pp. 98-103 ◽  
Author(s):  
KY Lei ◽  
AS Prasad ◽  
E Bowersox ◽  
D Oberleas

The study involved three levels of dietary zinc (deficient, marginal, and adequate) and four hormonal conditions; namely, no steriods, norethindrone, mestranol, and norethindrone plus mestranol. The steroids were incorporated into diets and fed to 11-wk-old female Sprague-Dawley rats. After 10 wk of treatment, various tissues were excised for mineral assays by atomic-absorption spectrophotometry. Both steroids, reduced weight gain. Mestranol depressed plasma zinc, tibia copper and magnesium, and liver iron, but elevated the zinc levels in liver and erythrocytes, plasma copper, liver magnesium and calcium, and iron content of tibia and heart. In general, the effect was most prominent with adequate zinc but diminished in magnitude with the reduction of zinc intake. In addition, norethindrone increased heart iron and tibia calcium. Mestranol appeared to be the main causative factor and may have induced a possible shift of minerals from one pool to another. As expected, zinc deficiency resulted in the reduction of zinc concentrations of plasma, tibia, kidney, and pancreas, and the elevation of copper, iron, magnesium, and calcium concentrations of various tissues.


1990 ◽  
Vol 78 (6) ◽  
pp. 547-549 ◽  
Author(s):  
Michael Barry ◽  
P. W. N. Keeling ◽  
John Feely

1. The zinc status and drug-metabolizing ability of 15 patients with histologically diagnosed hepatic cirrhosis were studied. Zinc status was assessed using both serum and leucocyte zinc concentrations, and drug-metabolizing ability was assessed by antipyrine kinetics. 2. Patients with cirrhosis were found to have lower serum and leucocyte zinc concentrations when compared with a healthy control group. 3. Leucocyte zinc content and antipyrine clearance were correlated. Those patients with the lowest leucocyte zinc content had the greatest impairment of drug metabolism. Antipyrine elimination and serum zinc concentrations were not correlated. 4. Leucocyte zinc concentrations and antipyrine clearance were not influenced by the severity of liver dysfunction, as assessed by using the Child Turcotte classification. 5. These results suggest that tissue zinc depletion in some patients with hepatic cirrhosis may explain in part the impaired capacity to metabolize drugs.


1980 ◽  
Vol 20 (102) ◽  
pp. 20 ◽  
Author(s):  
DG Masters ◽  
M Somers

Zinc status of grazing sheep was surveyed for three years on six properties in the south-west of Western Australia. The concentration of zinc in the plasma of rams and ewes varied both among sheep and among properties, and was up to 21% lower in autumn than in spring. The zinc status of ewes, but not rams, remained low in winter, as reflected by both plasma and wool levels. Pasture zinc levels were lowest in autumn and highest in winter, and regular recordings below 20 �g g-1 were made. The low zinc status of sheep in autumn was accompanied by low pasture zinc content and a low pasture availability. However, the data suggest that the decrease in maternal zinc levels during winter are due to reproductive stress. Plasma zinc levels regularly fell below the presently suggested optimum, and seasonal variation in both plasma and wool zinc levels indicates that in autumn and possibly winter there is an inadequate uptake of zinc. This is indirect evidence for a widespread marginal deficiency of zinc in grazing sheep.


1980 ◽  
Vol 95 (1) ◽  
pp. 135-139 ◽  
Author(s):  
J. Price ◽  
W. R. Humphries

SummaryTrials were conducted on 21 farms to examine the influence of supplementary zinc on growth rate of 978 beef cattle maintained on winter rations typical of N.E. Scotland.The concentration of zinc in the normal farm rations ranged from 13·3 to 32·1 mg/kg D.M. and half of the animals on trial on each farm received supplements providing an additional 60 mg Zn/kg D.M. Before supplementation, the farm mean plasma zinc concentrations varied from 0·73 to l·10mg Zn/l; these levels were not elevated by zinc supplementation.The differences in mean daily weight gain between zinc-supplemented and control cattle on individual farms during 100–140 days on trial ranged from –0·14 to +0·22 kg/day and were not related to plasma zinc concentration before supplementation or to the zinc content of the basal rations. The mean daily weight gain of heifers receiving supplementary zinc was significantly greater (P< 0·02) than that of the controls by 0·05 kg/day during the first 60–80 days only. Bulls and steers showed no response to supplementary zinc.


Author(s):  
Andrew G. Hall ◽  
Janet C. King ◽  
Christine M. McDonald

AbstractProgress improving zinc nutrition globally is slowed by limited understanding of population zinc status. This challenge is compounded when small differences in measurement can bias the determination of zinc deficiency rates. Our objective was to evaluate zinc analytical accuracy and precision among different instrument types and sample matrices using a standardized method. Participating laboratories analyzed zinc content of plasma, serum, liver samples, and controls, using a standardized method based on current practice. Instrument calibration and drift were evaluated using a zinc standard. Accuracy was evaluated by percent error vs. reference, and precision by coefficient of variation (CV). Seven laboratories in 4 countries running 9 instruments completed the exercise: 4 atomic absorbance spectrometers (AAS), 1 inductively coupled plasma optical emission spectrometer (ICP-OES), and 4 ICP mass spectrometers (ICP-MS). Calibration differed between individual instruments up to 18.9% (p < 0.001). Geometric mean (95% CI) percent error was 3.5% (2.3%, 5.2%) and CV was 2.1% (1.7%, 2.5%) overall. There were no significant differences in percent error or CV among instrument types (p = 0.91, p = 0.15, respectively). Among sample matrices, serum and plasma zinc measures had the highest CV: 4.8% (3.0%, 7.7%) and 3.9% (2.9%, 5.4%), respectively (p < 0.05). When using standardized materials and methods, similar zinc concentration values, accuracy, and precision were achieved using AAS, ICP-OES, or ICP-MS. However, method development is needed for improvement in serum and plasma zinc measurement precision. Differences in calibration among instruments demonstrate a need for harmonization among laboratories.


1979 ◽  
Vol 94 (4) ◽  
pp. 607-608 ◽  
Author(s):  
K. Michael Hambidge ◽  
Philip A. Walravens ◽  
Clare E. Casey ◽  
Ronald M. Brown ◽  
Connie Bender

2021 ◽  
Vol 11 (2) ◽  
pp. 21-28
Author(s):  
V.P. Novikova ◽  
◽  
A.A. Pokhlebkina ◽  
D.V. Zaslavsky ◽  
A.I. Khavkin ◽  
...  

Enteropathic acrodermatitis is a rare hereditary form of zinc deficiency, characterized by periorial and acral dermatitis, alopecia and diarrhea. Refers to congenital disorders of zinc metabolism, inherited as an autosomal recessive disease resulting from mutations in the gene for the zinc transporter SLC39A4. The prevalence ranges from 1 to 9:1,000,000, with an overall incidence of 1:500,000 newborns. The disease usually manifests itself in infancy, within a few weeks of stopping breastfeeding and switching the baby to a cow's milk-based formula, or in the first days of life if artificially fed from birth. The classical clinical manifestations of acrodermatitis enteropathic are characterized by the triad: acral and periofital dermatitis, alopecia and diarrhea, but all three signs together occur only in 20% of cases. Diarrhea may develop concurrently with skin symptoms, may precede or occur later. Characteristic signs of skin lesions include sharply demarcated, dry, scaly erythematous plaques or edematous foci with vesicles and pustules on the skin of the elbow and knee joints, distal extremities, genitals, in the inguinal folds, which are usually symmetrically distributed, have sharp boundaries and irregular outlines. The course of the skin syndrome is long, as it progresses, non-healing erosive and ulcerative areas appear. Plasma zinc deficiency is the gold standard for diagnosis. Most infants with AE have low plasma zinc concentrations (<500 mcg/L or <50 mcg/dl), but a level of less than 70 mcg/L on an empty stomach or less than 65 mcg/dl in older non-dieting children is considered diagnostically significant. Treatment for this disease usually includes enteral or parenteral zinc administration, at a dose of 1-3 mg/kg/day. for elemental zinc. A clinical response is observed within 5–10 days. Supportive zinc therapy is necessary throughout the patient's life, although periods of remission have been reported. Topical therapy is also used: Dexpanthenol in the form of a cream, applied 3 times a day in the area of dermatitis, can enhance re-epithelialization. There is no significant evidence of improvement with topical zinc application. No activity restrictions are required for patients with acrodermatitis enteropathic. Key words: zinc deficiency, enteropathic acrodermatitis, children


PEDIATRICS ◽  
1986 ◽  
Vol 77 (1) ◽  
pp. 132-133
Author(s):  
MICHAEL H. N. GOLDEN ◽  
BARBARA E. GOLDEN

To the Editor.— Kumar and Anday1 describe three premature infants presenting with edema and hypoproteinemia—the classical signs of kwashiorkor—between 5 and 9 weeks of age. Such cases are not uncommon in developing countries. Kumar and Anday's patients had low plasma zinc concentrations (43, 37, and 42 µg/dL). On this basis the authors claim that edema and hypoproteinemia is a clinical presentation of zinc deficiency not previously reported. We reported2 a clear association between "nutritional" edema and a low plasma zinc concentration in 1979; our subsequent experience has confirmed that edema of this type is always associated with a low plasma zinc concentration, as indeed Kumar and Andays' cases demonstrate.


1998 ◽  
Vol 133 (6) ◽  
pp. 761-764 ◽  
Author(s):  
Nancy F. Krebs ◽  
Marci Sontag ◽  
Frank J. Accurso ◽  
K.Michael Hambidge

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