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PubMed1985

Intestinal absorption and excretion of zinc in streptozotocin-diabetic rats as affected by dietary zinc and protein.

65Zn was used to examine the effects of dietary zinc and protein on true zinc absorption and intestinal excretion of endogenous zinc by an isotope dilution technique in streptozotocin-diabetic and control rats. Four groups each of diabetic and control rats were fed diets containing 20 ppm Zn, 20% egg white protein (HMHP); 20 ppm Zn, 10% egg white protein (HMLP); 10 ppm Zn, 20% egg white protein (LMHP); and 10 ppm Zn, 10% egg white protein (LMLP). Measurement of zinc balance was begun 9 d after an i.m. injection of 65Zn. True zinc absorption and the contribution of endogenous zinc to fecal zinc excretion were calculated from the isotopically labeled and unlabeled zinc in the feces, duodenum and kidney. Results from the isotope dilution study indicated that diabetic rats, but not control rats, absorbed more zinc from 20 ppm zinc diets than from 10ppm zinc diets and that all rats absorbed more zinc from 20% protein diets than from 10% protein diets. Furthermore, all rats excreted more endogenous zinc from their intestines when dietary zinc and protein levels resulted in greater zinc absorption. In diabetic and control rats, consuming equivalent amounts of zinc, the amount of zinc absorbed was not significantly different, but the amount of zinc excreted by the intestine was less in the diabetic rats. Decreased intestinal excretion of endogenous zinc may be a homeostatic response to the increased urinary excretion of endogenous zinc in the diabetic rats and may also lead to the elevated zinc concentrations observed in some organs of the diabetic rats.

Analysis of Variance↗
PubMed1999

The influence of zinc status on the kinetics of zinc uptake into cultured endothelial cells.

To better understand cellular zinc homeostasis and characterize the zinc transport process, a mammalian cell culture model was utilized to investigate the influence of zinc status on the kinetics of zinc uptake. Culturing conditions were optimized to induce moderate zinc deficiency and zinc excess while still sustaining the general health of the cells. Cells were grown in (1) control medium of 10% fetal bovine serum (FBS) in minimum essential medium (MEM; 5.0 micromol zinc/L), (2) low zinc medium (10% dialyzed FBS in MEM; 1.5 micromol zinc/L), or (3) zinc back medium (10% dialyzed FBS in MEM with zinc added as ZnCl(2); 5.0 micromol zinc/L). Bovine pulmonary artery endothelial cells (BPAEC), porcine aortic endothelial cells (PAEC), and porcine venous endothelial cells (PVEC) were evaluated as to their responsiveness to our zinc-deficient conditions. Zinc uptake was faster (P < 0.001) in all three cell types when they were grown in low zinc medium compared with controls; the increases were 32% in PAEC, 37% in PVEC, and 66% in BPAEC. Further kinetic analysis with BPAEC demonstrated a 31% increase (P < 0.05) in the maximum rate of zinc uptake (Jmax) grown in low zinc medium compared with controls, but no difference (P > 0.05) between the low zinc group and the control group in the concentration at which uptake was half-maximal (K). Zinc uptake into BPAEC grown in excess zinc conditions was not different (P > 0.05) unless the medium contained greater than 50 micromol zinc/L. In conclusion, BPAEC increased their ability for zinc uptake in response to moderate zinc deficiency, but did not change their kinetics of zinc uptake during moderate zinc excess.

Journal Article↗
PubMed2006

Zinc ions in the endocrine and exocrine pancreas of zinc deficient rats.

OBJECTIVE: Zinc deficiency is a problem world-wide. Zinc and insulin are intimately related, and a reduced zinc intake may affect glucose metabolism. The present study investigates how subclinical zinc deficiency in rats affects glucose metabolism and zinc distribution in the pancreas. METHODS: Glucose metabolism was evaluated by blood-glucose, serum insulin, homeostasis model assessment (HOMA), and intraperitoneal glucose tolerance tests. Immersion zinc-sulphide autometallography (iZnSAMG) was used to describe zinc ion distribution. RESULTS: After 4 weeks on a zinc deficient diet (<10 ppm), the zinc deficient rats had a slightly impaired glucose metabolism characterized by significantly increased blood-glucose levels. No differences in serum insulin, insulin resistance, beta-cell function were observed. The zinc deficient rats had significantly decreased serum zinc without any clinical signs of zinc deficiency. Zinc ion staining intensity of the islets of Langerhans was unaffected by the zinc deficiency. In contrast, the acinar cells in the exocrine pancreas appeared depleted of iZnSAMG grains in the zinc deficient rats when compared with their controls. Though statistically non-significant, a reduction in total zinc of the pancreas was found. CONCLUSIONS: The present findings suggest that the endocrine pancreas is able to compensate for the subclinical zinc deficiency as it maintains an adequate zinc ion level in the secretory vesicles for insulin storage. The exocrine pancreas lacks this ability; it exhibits decreased levels of zinc ion staining as a consequence of 4 weeks of reduced zinc intake.

Animal Feed↗
PubMed1992

Zinc uptake by blood cells of rats in zinc deficiency and inflammation.

In zinc deficiency, the function of leukocytes is impaired. However, the results of studies on the zinc concentration of blood cells in zinc deficiency are conflicting, probably in part because of technical and analytical problems. The aim of this study was to investigate, under standard conditions, the uptake of 65Zn-labeled zinc by blood cells, taken from zinc-deficient rats and from rats in which an inflammation is induced. In both conditions, the serum zinc concentration is reduced. In clinical practice, this makes it difficult to determine whether the decrease in serum zinc is the result of a real or an apparent zinc deficiency. In stress, like an inflammatory disease, the decrease of zinc reflects an apparent zinc deficiency because of redistribution of serum zinc into the liver and because of decrease in serum albumin concentration. Over 70% of the serum zinc is bound to albumin. Blood cells from zinc-deficient and control rats were isolated using a discontinuous Percoll gradient and incubated under nearly physiological conditions in a 65Zn-containing medium. A significant increase in the in vitro uptake of 65Zn-labeled zinc by the blood cells of zinc-deficient rats was seen: erythrocytes 1.3, mononuclear cells 2.0, and polymorphonuclear cells 2.6 times the control values. During inflammation, no change in 65Zn-labeled zinc uptake by erythrocytes and mononuclear cells was demonstrated after 2 d, although the serum zinc and albumin concentrations were decreased, but a small but significant increase in zinc uptake by polymorphonuclear cells was observed. This study of 65Zn uptake in vitro under standard conditions may prove of value for distinguishing in patients real zinc deficiency from apparent zinc deficiency owing to, e.g., stress, although additional experiments should be performed.

Animals↗
PubMed1980

Reactivation in vitro of zinc-requiring apo-enzymes by rat liver zinc-thionein.

The ability of rat liver zinc-thionein to donate its metal to the apo-enzymes of the zinc enzymes horse liver alcohol dehydrogenase, yeast aldolase, thermolysin, Escherichia coli alkaline phosphatase and bovine erythrocyte carbonic anhydrase was investigated. Zinc-thionein was as good as, or better than, ZnSO(4), Zn(CH(3)CO(2))(2) or Zn(NO(3))(2) in donating its zinc to these apo-enzymes. Apo-(alcohol dehydrogenase) could not be reactivated by zinc salts or by zinc-thionein. Incubation of the other apo-enzymes with near-saturating amounts of zinc as ZnSO(4), Zn(CH(3)CO(2))(2), Zn(NO(3))(2), or zinc-thionein resulted in reactivation of the apo-enzymes. With apo-aldolase zinc-thionein gave 100% reactivation within 30min. Reactivation by ZnSO(4) and Zn(CH(3)CO(2))(2) was complete and instantaneous. Zinc-thionein was somewhat better than Zn(NO(3))(2) in completely reactivating apo-thermolysin. With apo-(alkaline phosphatase) 43% reactivation was obtained with Zn(CH(3)CO(2))(2) and 18% with zinc-thionein. With apo-(carbonic anhydrase) zinc-thionein was better than ZnSO(4), Zn(CH(3)CO(2))(2) or Zn(NO(3))(2), with a maximal reactivation of 54%. That zinc was really being transferred from zinc-thionein to apo-(carbonic anhydrase) was shown by the fact that 2,6-pyridine dicarboxylic acid and 1,10-phenanthroline had minimal effects on the reactivation of apo-(carbonic anhydrase) when added after the incubation {[apo-(carbonic anhydrase)+zinc thionein]+chelator}, but inhibited reactivation when added before the incubation {apo-(carbonic anhydrase)+[zinc-thionein+chelator]}. These observations support the idea that zinc-thionein can function in zinc homeostasis as a reservoir of zinc, releasing the metal to zinc-requiring metalloenzymes according to need.

Alcohol Oxidoreductases↗
PubMed2003

Induction of the ZRC1 metal tolerance gene in zinc-limited yeast confers resistance to zinc shock.

Zinc is an essential nutrient but toxic to cells with overaccumulation. For this reason, intracellular zinc levels are tightly controlled. In the yeast Saccharomyces cerevisiae, the Zrc1 and Cot1 proteins have been implicated in the storage and detoxification of excess zinc in the vacuole. Surprisingly, transcription of ZRC1 is induced in zinc-limited cells by the zinc-responsive transcription factor Zap1. We show here that this increase in ZRC1 expression is a novel mechanism of zinc homeostasis and stress tolerance. Zinc-limited cells also express high levels of the plasma membrane zinc uptake transporters. As a consequence, when zinc-limited cells are resupplied with small amounts of zinc, large quantities quickly accumulate in the cell, a condition we refer to as "zinc shock." We show here that ZRC1 and its induction in zinc-limited cells are required for resistance to this zinc shock. Experiments using the zinc-responsive fluorophore FuraZin-1 as an indicator of vacuolar zinc levels indicated that Zrc1 is required for the rapid transport of zinc into the vacuole during zinc shock. We also present evidence that cytosolic zinc rises to higher levels in cells unable to sequester this excess zinc. Thus, the increase in ZRC1 expression occurs prior to the zinc shock stress for which this induction is important. We propose that this "proactive" strategy of homeostatic regulation, such as we document here for ZRC1, may represent a common but largely unrecognized phenomenon.

Carrier Proteins↗
PubMed1994

Marginal zinc deficiency in older adults: responsiveness of zinc status indicators.

OBJECTIVE: Suspicions that mild zinc deficiency is common among the elderly cannot be confirmed or refuted because definitive indicators of zinc status are lacking. The goal of this study was to document the clinical responsiveness of parameters of zinc status in a group of older adults consuming a carefully controlled diet: first moderately low in zinc (3.97 mg/day for 15 days) and then high in zinc (28.19 mg/day for 6 days). METHODS: Fifteen older adults (mean age = 66.6 yrs) volunteered to consume a marginally zinc-deficient diet for 15 days followed by 6 days of zinc repletion. Plasma concentrations of erythrocyte metallothionein and the enzyme 5'-nucleotidase, as well as levels of zinc, alkaline phosphatase, copper and ceruloplasmin were measured before and after zinc depletion and repletion. RESULTS: Plasma zinc levels were not altered during the study. Alkaline phosphatase (AP) values did not change in the expected direction, although a small decrease in AP following zinc repletion was statistically significant. Erythrocyte metallothionein results followed a pattern similar to that of alkaline phosphatase, little change, but a small, statistically significant drop after zinc repletion. As expected, there were no diet-associated changes in plasma copper and ceruloplasmin levels. In contrast, plasma concentrations of the enzyme 5'-nucleotidase decreased (p < 0.01) from 2.7 +/- 0.5 to 1.1 +/- 0.5 U during zinc depletion and increased (p < 0.05) to 2.2 +/- 0.4 U after 6 days of repletion. CONCLUSIONS: Mild zinc deficiency is difficult to detect. In this study, traditional indicators such as plasma zinc and alkaline phosphatase did not change as would be expected in response to alterations in zinc intake. Likewise, erythrocyte metallothionein did not respond to altered zinc intakes as expected but this factor may reflect long-standing or more severe zinc depletion and thus requires additional study. Activity of the enzyme 5'-nucleotidase appears responsive to acute changes in zinc intake; however, more work is needed to define how well these activities will reflect zinc intake in other types of subjects.

5'-Nucleotidase↗
PubMed1982

Neutrophil zinc: an indicator of zinc status in man.

At present there is no single laboratory test which establishes the diagnosis of zinc deficiency in human subjects. Neutrophils are rich in zinc and have a short life span in the peripheral blood. The possibility that neutrophil zinc may be a reliable indicator of zinc status was tested in this study. Experiments were carried out in two groups of subjects. The first group of subjects included sickle cell anemia patients, known to be zinc-deficient. Zinc concentrations in the plasma, erythrocytes, and neutrophils were assayed by means of flameless atomic absorption spectrophotometry in 17 males and 7 females between the ages of 14-19 years. Neutrophil zinc in sickle cell anemia subjects correlated significantly with height (r = 0.62, p less than 0.005), weight (r = 0.66, p less than 0.001), and serum testosterone in males (r = 0.71, p less than 0.01). Inasmuch as growth retardation and hypogonadism in male sickle cell anemia patients have been related to a deficiency of zinc, these results indicate that the neutrophil zinc assay may be a good indicator of zinc deficiency in human subjects. Such correlations were not observed with zinc levels in the plasma erythrocytes. In the second experiment, a marginal deficiency of zinc was induced in five healthy human volunteers between the ages of 45-65 years by administering a semipurified soy protein-based diet for 12 weeks with daily zinc intake of 14.3 +/- 1.01 mg according to previously published techniques. Zinc balance (excluding sweat loss) on the soy protein diet at the end of the experiment was negative (-2.39 +/- 0.79 mg/dl). At the end of 4 weeks on the experimental diet, neutrophil zinc (mean +/- S.D.) was 107 +/- 27.2 in comparison to the base line level of 135.33 +/- 3.54 micrograms/10(10) cells (p less than 0.05). Changes in plasma zinc at the end of 4 weeks of dietary treatment were not statistically significant. After 12 weeks on the experimental diet, the neutrophil zinc declined 30.87%. In conclusion, our studies in two human zinc-deficient models suggest that neutrophil zinc levels may be a reliable and sensitive indicator of zinc status.

Adult↗
PubMed1983

[Effect of different concentrations of various zinc complexes (picolinate, citrate, 8-hydroxyquinolate) in comparison with sulfate on zinc supply status in rats].

12 groups of 8 young male Sprague-Dawley rats received a semisynthetic casein-diet, whose zinc concentration (1.3 ppm) was adjusted to 5, 10 and 15 ppm by supplementation of various Zn complexes or salts like Zn citrate, Zn picolinate, Zn 8-hydroxyquinolate and Zn sulfate. After 24 days all animals were killed and examined on parameters of zinc supply status. The weight gain of the animals with 5 ppm dietary zinc was strongly reduced compared to groups with the higher dietary zinc content. The type of the supplemented Zn compound showed in no way an influence on the live-weight of the animals. The zinc concentration of the tissues, too, was only dependent on the level of the dietary zinc concentration and not on the type of supplemented zinc compound. The activity of the alkaline phosphatase in serum, a zinc metalloenzyme, was altogether reduced in the zinc-deficient animals with 5 ppm dietary zinc content, but showed a significant higher activity in the citrate and 8-hydroxyquinolate group than in the sulfate and picolinate group. Also the percent zinc-binding capacity of serum, a good indicator for estimating the zinc supply status of rats, showed a better zinc supply of the citrate group with 5 as well as 10 ppm dietary zinc, compared with the other groups on the same dietary zinc content. The serum zinc concentration of rats with 5 ppm as Zn citrate was more than twice higher than in animals given zinc as picolinate, 8-hydroxyquinolate or sulfate. The results indicate a better utilization of zinc chelated by citric acid than by picolinic acid, 8-hydroxyquinoline or as salt like sulfate. But the higher bioavailability of zinc in human milk should not only be attributed to the presence of citrate.

Alkaline Phosphatase↗
PubMedDate not supplied

Zinc tolerance test patterns in normal children and in moderate and severe zinc deficiency states.

Twenty-six normal, 38 moderately and 14 severely zinc-deficient children, aged 2-12 years, were examined by clinical and laboratory approaches. After fasting-blood sampling, 120 mg zinc sulphate (25 mg elemental zinc) were administered orally to each group of children, to obtain zinc tolerance curve patterns. Sampling proceeded to the 2nd and 4th hours of the loading-test period. Plasma zinc was assessed on an atomic absorption spectrophotometer. In normal children, at the 2nd hour of loading, a significant (p < .001) elevation (1.764 +/- 0.133 mg/l) in the mean (+/- SEM) plasma zinc level was noted; also at the 4th hour a significant (p < .001) decrease (1.506 +/- 0.123 mg/l) in the mean plasma zinc level was shown. The mean plasma zinc level at the 4th hour was found higher than the mean fasting plasma zinc level (1.054 +/- 0.061 mg/l), but lower than the mean level found at the 2nd hour. In moderately zinc-deficient children, the rise in the 2nd hour and the fall in the 4th hour in the plasma zinc level were highly significant (p < .001 and p < .001, respectively) in relation to fasting blood level. However, in severely zinc-deficient children, the intensity of the increase (0.746 +/- 0.147 mg/l) in plasma zinc level at the 2nd hour was of lesser significance (p < .006) and the fall (0.424 +/- 0.061) mg/l) at the 4th hour was not significant. Therefore, in children with normal plasma zinc levels, an increase of more than 0.50 mg/l was seen at the 2nd hour of loading. This rise was seen to persist at the 4th hour. However, in children with moderate zinc deficiency, although again an increase of 0.50 mg/l was seen at the 2nd hour this increase did not persist at the 4th hour; and the 4th-hour value showed a significant decrease in relation to the 2nd hour value. Whereas, in children with severe zinc deficiency the rise of plasma level at the 2nd hour was less than 0.5 mg/l and the fall at the 4th hour was to such a level which was not significant in relation to fasting zinc level. This could be due to enhanced uptake of zinc off the circulation by the depleted tissues in severe zinc deficiency.

Administration, Oral↗
PubMed2004

Zinc supplementation reduces fractional zinc absorption in young and elderly korean women.

BACKGROUND: Adjustments in zinc losses and absorption are thought to maintain zinc homeostasis with changes in intake, but the capacity to make these adjustments appears to be affected by aging. Zinc status of the individual may also influence adjustments in fractional zinc absorption. OBJECTIVE: The purpose of this study was to compare the effects of changes in zinc status due to zinc supplementation on fractional zinc absorption in young and elderly Korean women. DESIGN: Zinc status and absorption were measured initially in 15 young (20-24 yr) and 15 elderly women (64-75 yr) confined to a metabolic unit and consuming a typical Korean diet. Upon discharge from the unit the women were supplemented with 22 mg zinc/d for 28 days. On d 20, the women returned to the unit for measurement of zinc status and absorption. Fractional zinc absorption (FZA) was estimated from the same typical Korean breakfast at both time points using the dual isotopic tracer method. Zinc stable isotopic ratios were measured in urine samples collected for 3 days following isotope administration. RESULTS: Plasma and urinary zinc concentrations increased significantly with zinc supplementation in the young but not the elderly women. FZA decreased following zinc supplementation in the young women from 22 to 8% (p < 0.0001) and in the elderly women from 19 to 10% (p < 0.0001). The decline in young women was greater than that in elderly women (p < 0.05). CONCLUSIONS: Both young and elderly women reduced their efficiency of zinc absorption with zinc supplementation. But, plasma and urinary zinc concentrations did not increase in the elderly following zinc supplementation suggesting that age altered the use of the additional zinc.

Adult↗
PubMedDate not supplied

Effect of intragastric pH on the absorption of oral zinc acetate and zinc oxide in young healthy volunteers.

BACKGROUND: Zinc is an important nutrient and is necessary to maintain a multitude of physiologic processes. Mineral supplements that provide physiologic doses of zinc may be used when dietary zinc is inadequate. Zinc is also used in pharmacologic doses to treat zinc deficiency and diseases such as Wilson's disease and acrodermatitis enteropathica. Although there are several zinc salts available, they are not equal in solubility, which is thought to be a key factor in zinc absorption. Moreover, the solubility of the salts is affected by pH, which may vary between pH 1 and 7 under various physiologic conditions in the stomach. The objectives of this 2-way 4-phase crossover study were to evaluate the effect of high (> or = 5) and low (< or = 3) intragastric pH on the absorption of zinc from the acetate and oxide salt in young healthy volunteers. METHODS: After a 9-hour fast, 10 healthy subjects (5 males and 5 females) were given a single oral dose of 50 mg of elemental zinc as the acetate or the oxide salt and under either high or low intragastric pH conditions. In all phases, a Heidelberg capsule pH detector-transmitter was used to continuously monitor intragastric pH. During the high pH phases, single oral doses of famotidine 40 mg oral suspension were administered before the zinc to raise the intragastric pH above 5. Intragastric pH < or = 3 was maintained in the low pH phases. RESULTS: The mean plasma zinc area under the curve for zinc acetate at low pH (AL), zinc acetate at high pH (AH), zinc oxide at low pH (OL), and zinc oxide at high pH (OH) were 524, 378, 364, and 66 micrograms x h/dL, respectively. The highest zinc plasma concentrations occurred with the acetate salt at a low intragastric pH, while the lowest plasma concentrations occurred with the oxide salt at a high intragastric pH. The importance of pH to the dissolution of these salts was verified by in vitro tests. Twenty-four-hour urinary zinc excretion was the highest for the AL phase and lowest for the OH phase. CONCLUSION: This study indicates that intragastric pH and salt solubility-dissolution are important in the oral absorption of zinc. Specifically, the oxide salt is not an appropriate zinc salt to use in those patients with elevated intragastric pH.

Absorption↗
PubMed1998

Control of zinc transfer between thionein, metallothionein, and zinc proteins.

Metallothionein (MT), despite its high metal binding constant (KZn = 3.2 x 10(13) M-1 at pH 7.4), can transfer zinc to the apoforms of zinc enzymes that have inherently lower stability constants. To gain insight into this paradox, we have studied zinc transfer between zinc enzymes and MT. Zinc can be transferred in both directions-i.e., from the enzymes to thionein (the apoform of MT) and from MT to the apoenzymes. Agents that mediate or enhance zinc transfer have been identified that provide kinetic pathways in either direction. MT does not transfer all of its seven zinc atoms to an apoenzyme, but apparently contains at least one that is more prone to transfer than the others. Modification of thiol ligands in MT zinc clusters increases the total number of zinc ions released and, hence, the extent of transfer. Aside from disulfide reagents, we show that selenium compounds are potential cellular enhancers of zinc transfer from MT to apoenzymes. Zinc transfer from zinc enzymes to thionein, on the other hand, is mediated by zinc-chelating agents such as Tris buffer, citrate, or glutathione. Redox agents are asymmetrically involved in both directions of zinc transfer. For example, reduced glutathione mediates zinc transfer from enzymes to thionein, whereas glutathione disulfide oxidizes MT with enhanced release of zinc and transfer of zinc to apoenzymes. Therefore, the cellular redox state as well as the concentration of other biological chelating agents might well determine the direction of zinc transfer and ultimately affect zinc distribution.

Animals↗
PubMed2000

Supplementation with L-histidine during dietary zinc repletion improves short-term memory in zinc-restricted young adult male rats.

Zinc, an essential dietary element, modulates neurotransmission in brain regions associated with cognition. Cognitive dysfunction has been reported in offspring of female rats fed zinc-restricted diets during gestation and/or lactation. Studies on the cognitive effects of zinc restriction during young adulthood are limited. After a 3-wk period of dietary zinc restriction, male rats (71-75 d old) were repleted with zinc chloride alone, or zinc chloride supplemented with L-histidine, and short-term memory was measured using the Morris water maze. During restriction, zinc-restricted rats demonstrated significantly longer (86.0%) retrieval latencies than nonrestricted controls, and significantly lower liver (25.5%), bone (32.5%) and hippocampal (3.2%) zinc concentrations. During subsequent repletion, rats repleted with zinc chloride supplemented with L-histidine improved their retrieval latencies to the extent that they were no longer significantly different from controls by repletion d 3. This was associated with a return of hippocampal zinc concentrations to control values by repletion d 3. The mean retrieval escape latencies of the zinc chloride-repleted rats remained significantly prolonged (75.0%). Collectively, these data indicate the following: 1) feeding a zinc-restricted diet for 3 wk impairs short-term memory in young adult male rats, and 2) repletion with dietary zinc supplemented with L-histidine improves short-term memory function more efficiently than dietary zinc chloride alone. The latter point suggests that dietary zinc supplemented with L-histidine is more bioavailable to the brain than zinc provided as zinc chloride alone. These findings are important in that they highlight the importance of both dietary zinc formulation and the use of functional assessments in determining zinc nutriture.

Analysis of Variance↗
PubMed1998

The effect of zinc-supplemented bread consumption on school children with asymptomatic zinc deficiency.

BACKGROUND: Zinc deficiency has been seen in developing countries in which grain-based vegetable protein is consumed more often than animal protein. This study was done to emphasize the importance of zinc-fortified foods and to investigate bioavailability of zinc in zinc-fortified bread. METHODS: Serum zinc concentrations in healthy 7- to 11-year-old school children were determined. In 24 of 101 children serum zinc concentrations were below 65 micrograms/ul. These 24 children with asymptomatic zinc deficiency were divided into two equal groups. The 12 children with low serum zinc concentrations received the zinc-fortified bread providing 2 mg/kg/day elemental zinc acetate for 90 days (zinc-supplemented group), whereas the other 12 children received the same quality bread with no zinc fortification (control group). RESULTS: By the end of the period, the zinc-supplemented group had significantly higher serum and leukocyte zinc concentrations (p < 0.01) and the weight, serum albumin levels, and alkaline phosphatase increased (p < 0.01). Immune functions improved, evidenced by conversion of delayed hypersensitivity skin reactions. Zinc-fortified bread (2 mg/kg/day) caused no side effects or manifestations of zinc toxicity. CONCLUSIONS: The results indicate that the bioavailability of zinc in the bread is satisfactory. The use of zinc-fortified bread was found to be an economical and readily accessible method to eliminate zinc deficiency and to prevent further occurrence.

Alkaline Phosphatase↗
PubMed1989

Effect of low zinc intake on absorption and excretion of zinc by infants studied with 70Zn as extrinsic tag.

The effect of low dietary intake of zinc was studied in six normal infants with the use of 70Zn as an extrinsic tag. Of the two study formulas, one provided a zinc intake similar to that of customary infant formulas ("high" intake), whereas the other provided a "low" zinc intake. Two zinc absorption studies were performed with each formula (sequence: high-low-low-high). Extrinsically labeled formula was fed for 24 h and excreta were collected for 72 h. Zinc isotope ratios were determined by inductively coupled plasma mass spectrometry (ICP/MS). When zinc intake was high, net zinc absorption was 9.1 +/- 8.7% (mean +/- SD) of intake and net zinc retention was 74 +/- 91 micrograms/(kg.d). True zinc (70Zn) absorption was 16.8 +/- 5.8% of intake and fecal excretion of endogenous zinc was 78 +/- 56 micrograms/(kg.d). When zinc intake was low, net absorption of zinc increased significantly (P less than 0.001) to 26.0 +/- 13.0% of intake, but net retention was not significantly different at 42 +/- 33 micrograms/(kg.d). True absorption of zinc also increased significantly (P less than 0.001) to 41.1 +/- 7.8% of intake, whereas fecal endogenous zinc decreased (P less than 0.05) to 34 +/- 16 micrograms/(kg.d) during low zinc intake. Thus, infants maintain zinc balance in the face of low zinc intake through increased efficiency of absorption and decreased excretion of endogenous zinc.

Adaptation, Physiological↗
PubMed2002

Zinc absorption and exchangeable zinc pool sizes in breast-fed infants fed meat or cereal as first complementary food.

BACKGROUND: The aims of this study were to compare the absorption efficiency of zinc from rice cereal and meat, with and without human milk, in 7-month-old breast-fed infants and to compare the size of exchangeable zinc pools in the infants according to the assigned complementary food. METHODS: Fractional absorption of zinc was measured in male infants using extrinsic labeling with a stable isotope of zinc in a test meal of either pureed beef (n = 9) or iron-fortified infant rice cereal (n = 9). The effect on fractional absorption of the addition of human milk to each complementary food was measured in each infant with a second oral zinc isotope. Fractional absorption was measured using fecal monitoring of isotope excretion, and exchangeable zinc pool size was calculated from isotopic enrichment in urine. RESULTS: Fractional absorption of zinc did not statistically differ between the beef (0.41 +/- 0.11) and cereal (0.36 +/- 0.05) test meals, although the trend showed that beef had higher fractional absorption than cereal. The higher intake of zinc from the beef versus cereal test meal resulted in a 16-fold greater amount of absorbed zinc ( P = 0.0002). The addition of human milk caused significant decreases in fractional absorption of zinc (0.07 +/- 0.02, P = 0.01) and absorbed zinc (0.04 +/- 0.01 mg, P < 0.0001). The size of the exchangeable zinc pool did not differ according to group but was strongly correlated with mean daily zinc intake ( r = 0.72, P = 0.003). CONCLUSIONS: These results confirm that meat as a complementary food for breast-fed infants can provide a rich source of dietary zinc that is well absorbed. The significant positive correlation between zinc intake and exchangeable zinc pool size suggests that increasing zinc intake positively affects metabolically available zinc.

Animals↗