Volume 16, Number 3
Review Article
Zinc in Endocrinology
Masayuki Kaji, MD, PhD
From the Division of Endocrinology and Metabolism, Shizuoka Children's Hospital, Japan.
Address reprint request to the Division of Endocrinology and Metabolism, Shizuoka
Children's Hospital, 860 Urushiyama, Shizuoka 420-8660, Japan (Dr Kaji).
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Abstract
Zinc is an essential trace nutrient and has close interrelationships with endocrine
system. Zinc is required for activities of more than 300 enzymes that are important for
nucleic acid and protein synthesis and cell division. Zinc is essential for growth and
reproductive function. Zinc deficiency causes growth retardation and delayed sexual
development. Zinc supplementation is effective to promote growth and sexual development in
zinc-deficient children. Zinc is very important for spermatogenesis and stability of the
chromatin structure of the sperm. Marked alterations in zinc homeostasis are observed in
thyroid diseases and zinc deficiency impairs the metabolism of thyroid hormones. Diabetes
mellitus affects zinc homeostasis in many ways. In the presence of zinc, insulin molecules
assemble to a dimeric form in vivo and hexameric form in vitro. This
hexameric insulin is clinically used. Zinc deficiency is still a public health problem all
over the world.
Key Words: zinc, zinc deficiency, endocrine system, enzymes
Introduction
Zinc has close interrelationships with endocrine system, and is essential for normal
growth, reproductive function, thyroid function and favorable glucose metabolism.
Therefore, zinc deficiency causes growth retardation, delayed sexual maturation,
hypogonadism, thyroid dysfunction and impaired glucose tolerance.
Conversely, a lot of hormones appear to influence zinc status in the body.
In this paper, the interrelationships between zinc and growth, gonadal function,
thyroid function and glucose metabolism will be discussed.
Zinc and Growth
Zinc ion (Zn2+) was shown to be present in high concentrations in growth hormone (GH)
secretory granules of the somatotrophs by histochemical analysis of the anterior
pituitary.1 GH is synthesized and secreted into storage granules before its
release from the anterior pituitary. Zinc ion induces the dimerization of GH in the way
that two zinc ions associate per dimer of GH in a cooperative fashion. The Zn2+-GH dimer
is more stable than monomeric GH and the formation of the dimeric complex is considered to
be important for storage of GH in the secretory granule.2 It is not clear,
however, how zinc ion functions in the release of GH from the somatotrophs.
Zinc deficiency has been well known to affect GH metabolism and changes in the
concentration of GH has been shown to influence or to be associated with changes in the
concentrations of zinc in blood, urine, and other tissues.3 Aihara et al
reported that in patients with GH deficiency the mean plasma zinc concentration was within
normal limits before treatment, but was significantly reduced after 4-12 months of GH
administration, and urinary excretion of zinc was significantly higher than in the
controls before treatment and decreased significantly after GH therapy.4 Our
recent study revealed that hair zinc concentrations in patients with GH deficiency under
GH therapy were about 1.5 times as high as in the controls. We speculate that GH might
promote intestinal absorption of zinc and/or promote zinc uptake of hair root cells.5
On the other hand, in patients with acromegaly there was a negative correlation between
plasma zinc and serum GH levels, and a positive correlation between urinary zinc excretion
and serum GH levels, and after adenomectomy, zinc was observed to increase in plasma and
decrease in urine.4 These findings may reflect a negative zinc balance and
chronic mild zinc deficiency in some patients with GH deficiency on long-term GH therapy
and in untreated patients with acromegaly, and suggest an increased zinc requirement
during catch-up growth or overgrowth accelerated by GH.4 Zinc may be a limiting
factor in growth-regulating mechanisms by modulating both GH release and GH action.3
Growth retardation caused by zinc deficiency in humans was first reported by Prasad et
al in 1963. The patients had remarkably short stature and hypogonadism. They were shown to
have zinc deficiency by decreased zinc concentrations in plasma, erythrocytes and hair,
and studies with 65Zn revealed that plasma zinc turnover was greater, the 24-hour
exchangeable pool was smaller, and the excretion of 65Zn in stool and urine was less in
the growth-retarded subjects than in the controls.6 Further studies showed that
the rate of growth was greater in patients who received supplemental zinc as compared with
those receiving only an adequate animal protein diet.7 Since then, many cases
of marginal or moderate growth impairment in children with zinc deficiency as a
consequence of inadequate zinc intake have been reported from various parts of the world.8,9
It appears that zinc deficiency is prevalent throughout the world in both developed and
developing countries.7 Favier indicated that depending on the country, 5 to 30%
of children were suffering from moderate zinc deficiency, responsible for small-for-age
height.10 Those reports showed positive effects of oral zinc supplementation on
growth velocity in children with zinc deficiency.7-10
There have been a few reports concerning the relationship between zinc deficiency and
GH secretory insufficiency. Nishi et al described a 13-year-old Japanese boy with growth
disturbance who had partial GH deficiency due to chronic mild zinc deficiency. His diet
was low in animal protein and consisted primarily of rice and vegetables, because he
disliked meats, fish, eggs, and dairy products which were rich sources of zinc. His plasma
zinc level and GH responses to the pharmacological stimulation tests were low. After three
months of oral zinc supplementation, however, his growth velocity improved without GH
replacement therapy, and his plasma zinc levels and GH responses to those tests increased
to the normal range.11
It has been well known that zinc deficiency in pregnant women causes fetal growth
retardation. Kirksey et al revealed a significant correlation between maternal plasma zinc
concentrations measured at midpregnancy and birth weight.12 Neggers et al
reported that the prevalence of low-birth-weight (LBW) infants was significantly higher
(eight times) among women with serum zinc concentrations in the lowest quartile in early
pregnancy, independent of other risk factors.13 On the other hand, there have
been several studies that showed no association between maternal zinc nutriture and
pregnancy outcome.14,15 However, Tamura et al mentioned that if plasma zinc
concentrations were a reliable indicator of zinc nutriture in pregnant women, they should
have found a positive correlation between plasma zinc concentrations and the various
pregnancy outcome measures in their study.15 Because the measurement of plasma
zinc concentrations is not considered so much useful in estimating the marginal zinc
nutriture.16
There have been controversies on the effects of zinc supplementation in pregnant women
on pregnancy outcome.17-20 The incidences of LBW are very high in many African
and South Asian countries. For example, an estimated 40-50% of all live births in
Bangladesh are classified as LBW, 70-80% of which are the result of intrauterine growth
retardation (IUGR).20 Infants born with IUGR have higher mortality rates and
are at higher risk of growth retardation and poor cognitive development than are their
normal-birth-weight counterparts. Effective interventions aimed at preventing LBW are
therefore particularly important potential strategies for reducing childhood malnutrition
and improving infant health.20 Maternal zinc supplementation has been suggested
as one possible nutritional intervention during pregnancy to improve pregnancy outcome in
developing countries.21 Not a few studies revealed that zinc supplementation
during pregnancy reduced the incidence of IUGR.18,19 However, the results of
zinc-supplementation trials in pregnant women to improve pregnancy outcome are not
consistent, possibly reflecting the use of insufficient sample sizes or the fact that
populations have varying risks of LBW and zinc deficiency.20 Mahomed et al
conducted a double-blind prospective study to evaluate the effects of zinc supplementation
during pregnancy on pregnancy outcome in the United Kingdom and found that there were no
differences in gestational age, birth weight, neonatal abnormalities, and complications of
labor and delivery between mothers given a zinc supplement and those given a placebo.17
It is now speculated that zinc supplementation during pregnancy might be beneficial only
in populations that are zinc deficient and at high risk of poor fetal growth.20
Marginal zinc deficiency seems prevalent in infancy even in developed countries.
Michaelsen et al examined zinc intake and status in healthy term infants from birth to 12
months of age in Denmark, and found suboptimal zinc status in many subjects during late
infancy. They also reported that serum zinc level at 9 months was positively associated
with growth velocity during the period from 6 to 9 months.22
In 1993, Nakamura et al conducted the first age-matched control study which showed that
oral zinc supplementation was effective in improving the growth rate in short children
with marginal zinc deficiency. They reported that oral zinc supplementation induced
increases of serum insulin-like growth factor-I (IGF-I), osteocalcin and alkaline
phosphatase activity.16 On the contrary, Prentice reported that zinc
supplementation failed to show beneficial effects on height gain in Guatemalan children,
although the relatively short supplementation period of 25 weeks might have been
insufficient to detect subtle changes in growth velocity.23
We studied zinc status in short Japanese children with normal GH secretion using the
body zinc clearance test that was recommended to detect the marginal zinc nutriture, and
evaluated the effects of oral zinc supplementation for children with short stature. The
results of the study indicated that about 60% of short children had marginal zinc
deficiency, and that oral zinc supplementation was effective on height gain in short boys
with marginal zinc deficiency, but not in girls. We also revealed a significant
correlation between the body zinc clearance values and percent increases in the growth
velocity after oral zinc supplementation in the boys, indicating that the more severe the
degree of zinc deficiency, the more effective oral zinc supplementation was on height
gain.24 The reason of such a high incidence of marginal zinc deficiency in
Japanese short children may be mainly the recent prevalence of precooked foods, snacks and
convenience foods in their diets. Although the reasons for the difference in the effects
of oral zinc supplementation on growth velocity between both sexes are not clear, a study
by Castillo-Duran et al showed the similar results. They reported that oral zinc
supplementation improved the height gain of boys with idiopathic short stature, but the
therapy had no effect on the growth velocity of girls in Chile. They hypothesized that the
predominance of the X chromosome in females of Indian origin was the cause of the reduced
height gain for the females in their study.25 There is no conclusive evidence,
however, that oral zinc supplementation has no effect on height gain in girls.
The mechanism by which zinc deficiency causes growth disturbance has been
controversial. Zinc is required for activities of more than 300 enzymes (zinc
metalloenzymes), in which zinc is located at the active site, including DNA polymerase,
RNA polymerase and thymidine kinase. Because these enzymes are important for nucleic acid
and protein synthesis and cell division, zinc may be essential for growth. Furthermore,
several hundreds of zinc-containing nucleoproteins are probably involved in gene
expression of various proteins.7
Zinc deficiency may adversely affect GH production and/or secretion.11 Since
zinc has an important role in protein synthesis, IGF-I synthesis can be impaired by zinc
deficiency. Ninh et al reported that low IGF-I levels in zinc-deprived rats were closely
associated with decreased hepatic IGF-I gene expression and with a diminution of liver GH
receptors and circulating GH-binding protein (GHBP). They also suggested that decreased
hepatic GH receptors and/or GHBP concentrations might be responsible for the decline of
circulating IGF-I in zinc-deficient animals.26
The presence of a large amount of zinc in bone tissue suggests that zinc plays an
important role in the development of the skeletal system.3 Retardation of bone
growth is a common finding in various conditions associated with zinc deficiency. Zinc has
a stimulatory effect on bone formation and mineralization.27 Zinc is required
for alkaline phosphatase activity and the enzyme is mainly produced by osteoblasts whose
major function is to provide calcium deposition in bone diaphysis. The administration of
vitamin D3 or zinc produced a significant increase in bone alkaline phosphatase activity
and DNA content. Moreover, the effect of vitamin D3 administration to increase bone
alkaline phosphatase activity and DNA content was synergistically enhanced by the
simultaneous treatment with zinc.28 The receptors for 1,25-dihydroxyvitamin D3
were shown to have two zinc-fingers at the site of interaction with DNA.29 One
possible function of zinc is to potentiate the interaction of the 1,25-dihydroxyvitamin
D3-receptor complex with DNA at that site. Zinc also directly activates aminoacyl-tRNA
synthetase in osteoblasts, and it stimulates cellular protein synthesis. Moreover, zinc
has an inhibitory effect on osteoclastic bone resorption by suppressing osteoclast-like
cell formation from marrow cells.27
Zinc deficiency should be considered as an etiologic factor in some children with
unexplained short stature. Oral zinc supplementation should be considered as the
growth-promoting therapy for children with short stature once the status of their zinc
nutrition is established.
Zinc and the Gonads
The zinc content of the prostate gland, the seminal fluid and ejaculated sperm are very
high and testicular zinc is essential for spermatogenesis.30 The zinc content
of sperm increases after exposure to seminal fluid, suggesting that sperm accumulate zinc
as they traverse from the testicles to the urethra.31 Zinc is also involved in
a number of functions of importance to sperm physiology. Zinc supplied from the prostate
secures a high content of zinc in the sperm nucleus, that contributes to the stability of
the quaternary structure of the chromatin and preserves genomic integrity.32
Kvist et al found a positive relation between zinc in sperm nuclei and the resistance of
the chromatin to decondense when exposed to a detergent. They also observed that the
infertile men had lower degree of sperm chromatin stability and lower sperm zinc content
than the fertile donors did. A low content of nuclear zinc would impair the structural
stability of the chromatin and thereby increase the vulnerability of the male genome.32
Following contact with the oocyte, zinc removal from sperm appears to be involved in
penetration and fertilization.30 Zinc contributes to the stable attachment of
sperm head to tail, and its removal induces head-tail detachment.33 Once oocyte
penetration has taken place, the spermatozoan nucleus undergoes decondensation and forms
the pronucleus. This decondensation process requires reduction of the chromatin zinc
content, since zinc inhibits the process.34
In an in vitro study using rat testis tissues, the response of cyclic AMP and
testosterone to human chorionic gonadotropin (hCG) was found to be augmented by zinc ion
in the presence of calcium ion. This augmentation by zinc ion did not occur in the absence
of calcium ion, indicating that zinc ion acts synergistically with calcium ion and plays
an essential role in testicular function.35
Zinc deficiency causes atrophy of the seminiferous tubules, failure of spermatogenesis
and decreased testosterone secretion in the rat.30 McClain et al observed
appropriate responses of pituitary luteinizing hormone (LH) and follicle-stimulating
hormone (FSH) to gonadotropin-releasing hormone (GnRH) administration and insufficient
response of testosterone to hCG administration in zinc-deficient rats. They concluded that
the hypogonadism in zinc-deficient rats resulted mainly from Leydig cell failure, but not
from hypothalamo-pituitary dysfunction.36
Zinc deficiency impairs the responsiveness of Leydig cell to gonadotropins and may
cause primary hypogonadism in humans as well as in experimental animals. Abbasi et al
conducted a study of inducing zinc deficiency in men using zinc-restricted diet and found
that the baseline sperm concentration and total sperm count per ejaculate decreased
significantly after zinc restriction and returned to normal 6 to 12 months after zinc
supplementation. This study demonstrated that dietary restriction of zinc could affect
testicular function adversely.37 Hunt et al also observed the decreased serum
testosterone concentration and seminal volume per ejaculate in healthy male volunteers fed
zinc-restricted diet for 35 days.38
Another possibility of the relationship between zinc deficiency and hypogonadism has
been speculated. Steroid hormone receptors contain zinc-finger structures which function
as the DNA-binding domains of transcription factors. Zinc-finger is a structure in which
an atom of zinc is tetrahedrically coordinated to spatially conserved cysteines and
histidines and the zinc atom is absolutely required for binding to DNA.39
Therefore, zinc deficiency might impair the function of steroid hormone receptors and
consequently decrease the sex steroid action. However, there have been no clinical or
experimental data to support the hypothesis.
Human cases of hypogonadism caused by zinc deficiency were first reported by Prasad et
al in 1963. The male patients had severe hypogonadism coincidentally with markedly short
stature. The pubic hair appeared in all of them within 7 to 12 weeks after zinc
supplementation was started. The genitalia increased to normal size and secondary sexual
characteristics developed within 12 to 24 weeks in all of them.6
Zinc is also very important for female reproductive function and necessary for normal
ovulation and fertilization. Ronaghy and Halsted reported two female cases with short
stature and hypogonadism, who were treated with oral zinc administration and attained
catch-up growth and sexual development.40 Zinc deficiency in pregnancy is
associated with increased maternal morbidity, pregnancy-related toxemia, spontaneous
abortion, prolonged gestation or prematurity, inefficient labor, atonic bleeding, and
increased risks to the fetus: malformations and intrauterine growth retardation. These
different effects of zinc can be explained by its multiple action on the metabolism of sex
steroids, together with prostaglandins.41
Zinc was shown to inhibit prolactin secretion from the anterior pituitary. Brandao-Neto
et al studied the response of plasma prolactin to oral zinc administration in healthy male
and female adults, and observed that prolactin concentrations significantly decreased
below basal levels in response to the increase in plasma zinc levels in all the subjects.42
Although the inhibitory mechanism is not clear, zinc might affect the reproductive
function through the fluctuation of prolactin secretion in humans.
Zinc and the Thyroid
Marked alterations in zinc homeostasis were observed in patients with thyroid diseases.
In hyperthyroid patients, erythrocyte zinc content was shown to be significantly lower
than normal, and inversely related to plasma thyroxine concentration. Plasma zinc
concentration was, however, shown to be within normal range. Hyperthyroid patients
excreted significantly greater amounts of zinc than controls, indicative of a catabolic
process. This increased urinary loss might reflect a shift in the distribution of plasma
zinc between ultrafilterable fraction and zinc-albumin complexes. On the other hand, in
hypothyroid patients erythrocyte zinc content was shown to be significantly higher than
normal, and plasma zinc concentration, leukocyte zinc content and urinary zinc excretion
were lower than normal.43,44
Yoshida et al measured erythrocyte zinc concentrations in 28 healthy volunteers and 46
patients with hyperthyroidism, and observed a significant negative correlation between the
concentrations of erythrocyte zinc and those of both plasma thyroxine (T4) and
triiodothyronine (T3). They also revealed that after the treatment of 17 hyperthyroid
patients with antithyroid drugs, both mean plasma T4 and T3 concentrations became normal
within four weeks, but the normalization of erythrocyte zinc concentrations lagged about
two months behind them. The erythrocyte zinc concentrations significantly correlated with
both the plasma T4 and T3 concentrations obtained 0, 4, 8 and 12 weeks prior to the
erythrocyte sampling, and the highest correlation was observed between the erythrocyte
zinc concentrations and the plasma T4 and T3 concentrations measured 8 weeks previously.
Therefore, they suggested that erythrocyte zinc concentration in hyperthyroid patients
reflected the patients' mean thyroid hormone levels over the preceding several months.45
Zinc deficiency was shown to impair the metabolism of thyroid hormones. Kralik et al
reported that male Sprague-Dawley rats fed low-zinc diet for 40 days showed decreased
serum concentrations of T3 and free T4 by approximately 30% compared with those fed
adequate-zinc diet.46 Wada and King measured basal metabolic rate and plasma
thyroid hormones in healthy young men fed low-zinc diet for 54 days and thereafter fed
adequate-zinc diet for 9 days. They observed that basal metabolic rate and serum free T4
levels decreased significantly during the low-zinc period, and increased during
adequate-zinc period.47
Effects of zinc supplementation on thyroid function have been evaluated under some
pathological states. Arreola et al reported that oral zinc supplementation increased
plasma levels of TSH, T3, T4 and zinc in uremic patients under peritoneal dialysis, who
had been zinc-deficient at the beginning of the study. They also revealed a close
correlation between the changes in plasma zinc levels and the changes in TSH, T3 and T4
levels, suggesting that zinc deficiency might play a role in the biosynthesis or release
of hormones of the hypothalamic-pituitary-thyroid axis in chronic renal failure.48 Nishiyama
et al evaluated the effects of zinc supplementation on thyroid function in disabled
patients with mild to moderate zinc deficiency who had low serum free T3 and normal serum
T4 levels and showed enhanced reaction of serum TSH after TRH injection. They reported
that oral zinc supplementation for 12 months resulted in normalization of the serum free
T3 levels and the TRH-induced TSH reactions. They suggested the contribution of zinc to
conversion of T4 to T3 in humans.49
It is well known that thyroid dysfunction is common in patients with Down syndrome. It
was also shown that a marginal, but biologically relevant, zinc deficiency was usually
present in children with Down syndrome.50 Several studies were conducted to
evaluate the effects of zinc supplementation on thyroid function in Down syndrome, and
they revealed the positive effects to various extents.51,52 Bucci et al
evaluated the role of zinc deficiency in subclinical hypothyroidism and the changes of
thyroid function in children with Down syndrome cyclically supplemented with zinc sulfate.
Inverse correlations were observed between serum zinc and TSH levels; higher TSH levels
were found in hypozincemic patients at the beginning of the study. After six months of
oral zinc supplementation, an improvement of thyroid function was observed in hypozincemic
patients. At the end of the study after the second cycle of zinc supplementation, TSH
significantly decreased in treated hypozincemic patients and it was no longer different in
comparison to normozincemic patients.53
It is suggested that zinc has an inhibitory effect on calcitonin secretion from thyroid
tissue. Nishiyama et al observed that zinc infusion resulted in a decrease in serum
calcitonin concentration, but did not change the concentrations of ionized calcium and
parathyroid hormone in patients with short stature and insulin-dependent diabetes
mellitus, and in age-matched controls.54 The mechanism, however, remains to be
elucidated.
Since thyroid hormone receptors contain zinc-finger structures alike to steroid hormone
receptors, it has been speculated that zinc deficiency might cause insufficient thyroid
hormone action. However, there have been no clinical or experimental data to support the
hypothesis.
Zinc and Glucose Metabolism
Diabetes mellitus affects zinc homeostasis in many ways. It was revealed by a number of
studies that urinary zinc excretion was higher in diabetic patients, either type I or type
II, than in control subjects.55,56 The hyperzincuria was suggested to be a
result more of hyperglycemia than any specific effect of insulin on the renal tubule.57
El-Yazigi et al found a positive correlation between urinary zinc excretion and blood
hemoglobin A1c levels.58 The mechanism of hyperzincuria in diabetic patients,
however, remains unclear.
While several studies observed that plasma zinc levels were lower in diabetic patients
than in control subjects,55,59 others showed there were no significant
differences between them.56 With respect to specific diabetes-associated
complications, there were no significant differences in plasma zinc concentrations nor
erythrocyte copper-zinc superoxide dismutase activities between diabetic patients with
retinopathy, hypertension or microvascular disease and those without any complications.55
Insulin molecule is produced by the ß-cell of the pancreatic islets. In the presence
of zinc within the cell, insulin monomers assemble to a dimeric form for storage and
secretion as the zinc crystal. In vitro, in the presence of zinc and at neutral pH,
dimeric insulin assembles further into a hexamer consisting of three dimeric units. This
form of insulin is relatively stable and it is this hexameric crystal which is the
commonly used pharmacologic form. As early as 1930s, when insulin was just becoming
available for commercial use, zinc was being added in vitro to make protamine zinc insulin
and lente crystalline insulin which prolonged the duration of action of the insulin by
delaying its absorption from the subcutaneous injection site thus requiring fewer insulin
injections.57 Inasmuch as zinc plays an important role in the synthesis,
storage and secretion of insulin as well as conformational integrity of insulin in the
hexameric form, zinc deficiency may adversely affect the ability of the islet ß-cell to
produce and secrete insulin.57
It was shown that a zinc-deficient diet induced a diabetic glucose tolerance in
experimental animals.60 It has been controversial whether low zinc intake
affects the onset and/or deterioration of diabetes in humans. Haglund et al evaluated the
association between the onset of type I diabetes and zinc intake from drinking water in
Swedish children. They designed a case-control study comparing diabetic patients and
control subjects with estimates of zinc contents of groundwater obtained in biogeochemical
samples from areas of residence, and observed that a high groundwater concentration of
zinc was associated with a significant decrease in risk of the onset of diabetes.
Moreover, in small rural areas, in which drinking water was taken from local wells and
thus was closely associated with the groundwater content within the area, an even stronger
association between zinc and diabetes was found. They concluded that a long-term exposure
to drinking water with a low zinc content could contribute to the disease occurrence
unless sufficiently compensated by dietary zinc.61
The etiology of type I diabetes is considered to be the result of autoimmune attack on
the islet ß-cell with subsequent destruction of the cell. One proposed mechanism by which
immune processes damage the cell is through cytokine-mediated induction of intracellular
oxidizing agents, particularly free radicals. Because zinc is an essential factor in a
variety of antioxidant enzymes, including superoxide dismutase, catalase and peroxidase,
zinc deficiency might be expected to contribute to the cellular damage observed in
diabetes.62 Several of the complications of diabetes may be related to
increased intracellular oxidants and free radicals associated with decreases in
intracellular zinc and in zinc-dependent antioxidant enzymes.57
The role of zinc in the clinical management of diabetes, its complication, or its
prevention is unclear.57 Although there have been some trials of zinc
supplementation to diabetic patients expecting the amelioration of the disease, they have
not been successful.56,59
Conclusion
Changes in zinc nutriture, especially zinc deficiency affects the endocrine system in
many ways, and a lot of hormones influence zinc status in the body. Various symptoms with
zinc deficiency mainly derive from impaired activities of zinc enzymes and dysfunction of
zinc-containing proteins.
Various degrees of zinc deficiency have been the public health problem all over the
world, especially for children and pregnant women. Caulfield et al mentioned that there
was considerable evidence that a high percentage of women worldwide consume diets
inadequate in zinc. They estimated, albeit grossly, that 82% of pregnant women in the
world had usual intakes of zinc inadequate to meet the normative needs of pregnancy and
the prevalence might be near 100% in developing countries.21 Even in developed
countries, marginal zinc deficiency is prevalent. We showed that about 60% of Japanese
children with short stature had marginal zinc deficiency. The reason of such a high
incidence of marginal zinc deficiency in Japanese children may be mainly the recent
prevalence of precooked foods, snacks and convenience foods in their diets.24
Nutritionists and physicians, especially pediatricians and obstetricians should be
concerned about zinc nutriture of children and pregnant women, and should designate them
appropriate diets with sufficient zinc contents.
References
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