Marginal Zinc Deficiency Research Articles

Zinc Supplementation of Pregnant Rats with Adequate Zinc Nutriture Suppresses Immune Functions in Their Offspring

The knowledge about consequences of marginal zinc (Zn) deficiency and Zn supplementation during pregnancy on immune function in the offspring is limited. The aim of this study was to examine whether effects of mild Zn deficiency and subsequent Zn supplementation during pregnancy persist after weaning and affect immune function of the offspring. Adult female rats were fed a Zn-adequate diet (ZC, n = 8) or a Zn-deficient diet (ZD, n = 8) from preconception through lactation. Pregnant rats were supplemented with either Zn (1.5 mg Zn in water) or placebo (water) 3 times/wk throughout pregnancy. Pups were orally immunized with cholera toxin and bovine serum albumin-dinitrophenol (DNP) 3 times at weekly intervals and killed 1 wk after the last dose. Proliferation and cytokine responses in lymphocytes from Payer’s patches and spleen, and antigen specific antibodies in serum were studied. Zn supplementation of ZD dams led to enhanced lymphocyte proliferation and IFN-γ responses in pups ZDZ+. In contrast, Zn supplementation of ZC dams suppressed these responses in pups ZCZ+. Total and DNP-specific IgA responses were lower in pups of the Zn-deficient group compared with the Zn-adequate group. Relative thymus weight was greater in the pups (ZDZ−) of ZD placebo-supplemented dams compared with the other groups at 31 d of age. Prepregnancy and early in utero Zn deficiency affected IgA responses in pups that could not be restored with Zn supplementation during pregnancy. Zn supplementation of ZC dams induced immunosuppressive effects in utero that may also be mediated through milk and persist in the offspring after weaning.

Hepatic Responses to Dietary Stress in Zinc- and Metallothionein-Deficient Mice

Metallothionein (MT) and zinc are both reported to be protective against oxidative and inflammatory stress and may also influence energy metabolism. The role of MT in regulating intracellular labile zinc, thus influencing zinc (Zn)-modulated protein activity, may be a key factor in the response to stress and other metabolic challenges. The objective of this study was to investigate the influence of dietary zinc intake and MT on hepatic responses to a pro-oxidant stress and energy challenge in the form of a high dietary intake of linoleic acid, an omega-6 polyunsaturated fatty acid. Male MT-null (KO) and wild-type (WT) mice, aged 16 weeks, were given semisynthetic diets containing 16% fat and either 5 (marginally zinc-deficient [ZD]) or 35 (zinc-adequate [ZA]) mg Zn/kg. For comparison, separate groups of KO and WT mice were given a rodent chow diet containing 3.36% fat and 86.6 mg Zn/kg. After 4 months on these diets, the body weights of all mice were equal, but liver size, weight, and lipid content were much greater in the animals that consumed semisynthetic diets compared to the chow diet. The increase in liver size was significantly lower in ZA but not ZD KO mice, compared with WT mice. Principally, MT appears to affect the diet-induced increase in liver tissue but it also influences the concentration of hepatic lipid. Plasma levels of C-reactive protein (CRP), a marker of inflammation, were increased by zinc deficiency in WT mice, suggesting that marginal zinc deficiency is proinflammatory. CRP was unaffected by zinc deficiency in KO mice, indicating a role for MT in modulating the influence of zinc. Neither zinc nor MT deficiency affects the level of soluble liver proteins, as determined using two-dimensional (2D) gel proteomics. This study highlights the close association between zinc and MT in the manifestation of stress responses.

Zinc status, psychological and nutritional assessment in old people recruited in five European countries: Zincage study

The paper shows the results on the relationship between zinc status, psychological dimensions (cognitive functions, mood, perceived stress) and nutritional aspects in European healthy old subjects recruited for ZINCAGE Project (supported by the European Commission in the Sixth Framework Programme). The old healthy subjects were recruited in Italy, Greece, Germany, France, Poland taking into account the different dietary habits between Northern and Southern European Countries and the pivotal role played by zinc for psychological functions. Measures of the cognitive status, mood and perceived stress level were obtained at baseline, using the "Mini Mental State Examination (MMSE)"; the "Geriatric Depression Scale (GDS - 15 items)" and the "Perceived Stress Scale (PSS)", respectively. Nutritional status was assessed using "Frequency Food Questionnaire". The sample included 853 old subjects, classified in 4 groups of age: 60-69-years-old (n = 359); 70-74-years-old (n = 225); 75-79-years-old (n = 153); 80-84-years-old (n = 116). Subjects were studied on the basis of plasma zinc, in which zinc </=11 microM means marginal zinc deficiency. The total samples showed that the 82% had no cognitive decline, whereas 76% presented a low GDS value indicating no depression. However, all psychological variables were related to plasma zinc values and nutritional assessment. In particular, a relationship between marginal zinc deficiency and impaired psychological dimensions occurred in Greece than in other European countries due to low intake and less variety of foods rich of zinc. This phenomenon was independent by the age, suggesting that a correct zinc intake from a wide range of foods may be useful to maintain a satisfactory plasma zinc levels as well as psychological status in elderly with subsequent achievement of healthy ageing.

Correlation between zinc status and immune function in the elderly

Zinc is essential for the immune system and elderly people have an increased probability for zinc deficiency, documented by a decline of serum or plasma zinc levels with age. Although most healthy elderly are not classified as clinically zinc deficient, even marginal zinc deprivation can affect immune function. Several striking similarities in the immunological changes during aging and zinc deficiency, including a reduction in the activity of the thymus and thymic hormones, a shift of the T helper cell balance towards TH2, decreased response to vaccination, and impaired functions of innae immune cells indicate that a wide prevalence of marginal zinc deficiency in elderly people may contribute to immunosenescence. Studies with oral zinc supplementation show the potential to improve the immune response of elderly people by restoration of the zinc levels, showing that balancing the zinc status may be a way to healthy aging. This review summarizes the current literature about zinc supplementation in the elderly and thereby defines the rationale for the immunological part of the ZINCAGE project.

Marginal Zinc Deficiency Increased the Susceptibility to Acute Lipopolysaccharide-Induced Liver Injury in Rats

Lipopolysaccharide (LPS) triggers a global activation of inflammatory responses leading to liver injury in humans. Zinc pretreatment has been shown to prevent LPS-induced hepatic necrosis. In North America, suboptimal zinc status is more common than once realized. However, the effect of inadequate zinc nutrition on the host's susceptibility to LPS-induced liver injury is not known. The objective of this study was to determine whether marginal zinc deficiency would render rats more susceptible to LPS-induced liver injury. Weanling Sprague-Dawley rats were assigned to one of three dietary treatment groups: marginally low zinc ad libitum (Z3; 3 mg zinc/kg diet), adequate zinc ad libitum (Z30; 30 mg zinc/kg diet), or adequate zinc pair-fed (Z30P) group. After 6 weeks, each dietary treatment group was further divided into LPS-control (saline) groups (C-Z3, C-Z30P, C-Z30) and LPS-treatment (1 mg/kg body weight, intraperitoneal, 8 hrs) groups (LPS-Z3, LPS-Z30P, LPS-Z30). LPS reduced the serum zinc concentration and increased the liver zinc concentration regardless of dietary zinc intake. Serum alanine aminotransferase level was higher in the LPS-Z3 rats than in the LPS-Z30P and LPS-Z30 rats. LPS also induced hepatocyte necrosis and neutrophil infiltration into the liver sinusoids. This LPS-induced liver damage was more severe in the LPS-Z3 rats than in the LPS-Z30P and LPS-Z30 rats. Together these findings have demonstrated that marginal zinc deficiency increased the susceptibility to LPS-induced liver injury in rats. These results indicate that patients with sepsis who have suboptimal zinc nutrition status may be at higher risk of developing greater liver damage.

Marginal Zinc Deficiency Exacerbates Bone Lead Accumulation and High Dietary Zinc Attenuates Lead Accumulation at the Expense of Bone Density in Growing Rats

Environmental lead exposure is associated with reduced bone growth and quality, which may predispose to osteoporosis. Zinc supplementation may reduce lead accumulation; however, effects on bone development have not been addressed. Our objective was to investigate the effects of marginal zinc (MZ) and supplemental zinc (SZ) intakes on bone lead deposition and skeletal development in lead-exposed rats. In a factorial design, weanling Sprague-Dawley rats were assigned to MZ (8 mg/kg diet); zinc-adequate control (CT; 30 mg/kg); zinc-adequate, diet-restricted (DR; 30 mg/kg); or SZ (300 mg/kg) groups, with and without lead acetate-containing drinking water (200 mg Pb/l) for 3 weeks. Excised femurs were analyzed for bone mineral density (BMD) by dual-energy x-ray absorptiometry, morphometry, and mineral content. MZ had higher femur lead and lower femur zinc concentrations and impaired skeletal growth and mineralization than CT. DR inhibited growth but did not result in higher femur lead concentrations than CT. SZ had higher femur zinc and lower femur lead concentrations than the other treatments. DR and SZ had impaired BMD versus CT and MZ. Lead also retarded skeletal growth and impaired BMD, but an interaction between lead and MZ was only found for femoral knee width, which was lower in MZ exposed to lead. In summary, while MZ deficiency exacerbated bone lead concentration, it generally did not intensify lead toxicity. SZ was protective against bone lead but was detrimental to BMD, suggesting that the optimal level of SZ to reduce lead absorption, while supporting growth and bone development, requires further investigation.

A proteomic analysis of aortic proteins in zinc and metallothionein deficiency

The objective of this work was to identify proteins and protein interactions that are modified by zinc and metallothionein (MT) deficiency in rodent aorta, using 2D gel proteomics. In one set of studies, 3-week old male rats were given either acutely (<1 mg Zn/kg) or marginally (6 mg Zn/kg) zinc deficient semi-synthetic diets for 5–6 weeks. Controls rats consumed a zinc-adequate diet (35 mg Zn/kg) and animals pair-fed with acutely deficient rats also consumed the adequate diet. Protein expression profiles in aorta were determined using 2D gel proteomics. In a second set of studies, aortic protein expression in adult male mice with a targeted disruption of the MT-1 and MT-2 genes and appropriate controls (both genotypes on a 129Sv genetic background) was studied using 2D gel proteomics. In the rat studies, both marginal and acute zinc deficiency decreased the level of aortic proteins associated with carbohydrate metabolism and lipid biosynthesis. Acute zinc deficiency also suppressed proteins related to the cytoskeleton. Although MT deficiency also decreased cytoskeleton-related protein levels, it increased levels of some enzymes relating to carbohydrate/energy metabolism. Principal Component Analysis followed by correlation analysis revealed key proteins affected by MT deficiency. These included small GTP-binding and related proteins. All authors except ISK were funded by the Scottish Executive Environment and Rural Affairs Department. ISK was funded by the Korean Ministry of Health and Welfare, grant # 03-PJ1-PG3-22000-0044.

Zinc deficiency and the prolonged accumulation of zinc in wounds.

Zinc is required for protein synthesis and therefore for wound healing. Zinc levels were 50 per cent higher in muscle and skin from abdominal wounds of rats during the maturation phase of wound healing, but mild deficiency greatly reduced this accumulation. The results suggest that zinc takes part in the late stages of wound healing when protein is laid down, and that such extra local demands expose otherwise marginal zinc deficiency.

Hyper- or Hypoleptinemia in Subjects with Zinc Deficiency?; Leptin Expression and Food Intake in Acute and Marginal Zinc Deficiency

Hyper- or Hypoleptinemia in Subjects with Zinc Deficiency?; Leptin Expression and Food Intake in Acute and Marginal Zinc Deficiency

Zinc Nutritional Status in Korean Adults from Rural, Urban and Metropolitan Areas

The zinc intake and status of South Koreans from rural, urban and metropolitan areas were compared to evaluate the zinc nutritional status in different regional areas in South Korea. The dietary habits of 721 healthy adult subjects (271 from rural, 240 from urban, 210 from metropolitan city) with an age range 30～64 (mean age 54±18) were assessed using a food frequency questionnaire. Mean daily Zn intake for rural, urban, and metropolitan areas was 6.5 mg, 7.3 mg, and 11.4 mg (p＜0.05), respectively, which was 54%, 61% and 95% of the Korean RDA for man (12 mg/d). Mean phytate : zinc molar ratios for rural, urban, and metropolitan city were 41, 34, and 30, respectively (p＜0.05), which were higher than the cutoff level of 20 for poor zinc status. The zinc intake and phytate : Zn molar ratio in the rural area were 0.5 and 1.3-fold compared to those of the metropolitan city, which can cause poor zinc nutriture in the rural area. Most of the zinc biomarkers were lower in the rural area than in the metropolitan city (p＜0.05) (mean rural and metropolitan values for plasma Zn: 80.8 μg/dL and 119.8 μg/dL, respectively; RBC Zn: 7.8 μg/dL and 8.8 μg/dL, respectively; plasma alkaline phosphatase (ALP) activity: 87 mU/mL and 100.4 mU/mL, respectively). It seems that a lower zinc intake in the rural area decreased zinc biomarker levels, such as plasma and RBC zinc, and plasma alkaline phosphatase activity, and caused the poor zinc nutritional status in this area. Most of the zinc biomarkers, such as RBC zinc and urinary and plasma zinc levels, in the subjects from the three localities, were within the normal range even when zinc intake of rural and urban subjects was low. The exception was plasma ALP activity in the rural area, which was lower than the reference level. Thus, marked zinc deficiency in these subjects were not observed, however, the potential for marginal zinc deficiency should be considered, especially for the rural area, because of the low zinc intake and the biomarker levels for marginal zinc deficiency.

Zinc Intake and Status of the Selected Korean Adults

Zinc intake and status of South Koreans from rural, urban and metropolitan areas were investigated. The dietary habits of 760 healthy male and female adult subjects with a mean age of 54 were assessed using a food frequency questionnaire and were verified using 24 h dietary recall. Daily Zn intakes for men and women were 7.4±5.4 mg and 7.0±5.4 mg, respectively, which were 62% and 70% of the Korean RDA. The phytate : zinc and phytate×calcium : zinc molar ratios were 38 and 398, respectively. Both the low intake of zinc and the high extremely phytate and phytate×calcium ratios with zinc suggest that South Koreans may be at risk of zinc deficiency. Plasma zinc (86±61 μg/dL), urinary zinc (33±27 μg/dL) and plasma alkaline phosphatase (102±52 mU/mL) levels within the normal range did not however suggest marked zinc deficiency in these subjects. However, conventional zinc biomarkers are known to be unreliable for assessment of marginal zinc deficiency. Based on zinc intake alone, it is likely that at least a proportion of these subjects were marginally zinc deficient and the wider consumption of zinc rich, phytate deficient foods, particularly in rural areas, would be beneficial.

Low zinc intake decreases the lymphatic output of retinol in rats infused intraduodenally with β-carotene

Previously, we have shown that the lymphatic absorption of retinol is significantly decreased in rats fed a low zinc diet. This study was conducted to determine whether the absorption of β-carotene also is altered in zinc-deficient male rats. The absorption of β-carotene was estimated by determining the amount of retinol appearing in the mesenteric lymph during intraduodenal infusion of β-carotene. One group of rats was fed the AIN-93G diet but low in zinc (LZ; 3 mg/kg) and the other was fed the same diet adequate in zinc (AZ; 30 mg/kg). The LZ and AZ rats were trained to meal feed equal amounts of the diets twice daily. At 6 weeks, each rat with lymph cannula was infused via an intraduodenal catheter at 3 ml/h for 8 h with a lipid emulsion containing 65.0 nmol β-carotene, 565.1 μmol triolein, 27.8 kBq 14C-triolein ( 14C-OA), 72 mg albumin, and 396 μmol Na-taurocholate in 24 ml PBS (pH, 6.7). The lymphatic output of retinol over the 8-h period was significantly lower in LZ rats than in AZ rats. The absorption of 14C-OA also was significantly lower in LZ rats. No significant differences were observed between groups in intestinal β-carotene 15,15′-dioxygenase, retinal reductase, and retinal oxidase activities. The findings demonstrate that low zinc intake or marginal zinc deficiency significantly lowers the absorption of β-carotene as estimated by lymphatic retinol output. The results also indicate that the decrease in retinol output in LZ rats is not linked to defects in β-carotene cleavage and subsequent conversion of retinal to retinol in the intestinal mucosa. This study suggests that zinc status is an important factor determining the intestinal absorption of β-carotene and hence the nutritional status of vitamin A.

Influence of dietary zinc deficiency during development on hepatic CYP2C11, CYP2C12, CYP3A2, CYP3A9, and CYP3A18 expression in postpubertal male rats

The present study investigated the effect of dietary zinc deficiency during the developmental period on hepatic cytochrome P450 (CYP) expression in postpubertal male rats. Twenty-one-day-old weanling male Wistar rats were randomly assigned to one of the following dietary groups: zinc-adequate (31 mg zinc/kg diet); marginal zinc-deficient (3 mg zinc/kg diet); severe zinc-deficient (1 mg zinc/kg diet); or pair-fed control for either the marginal or severe zinc-deficient group. All rats were killed at 63 days of age. Compared with the corresponding pair-fed controls, marginal zinc deficiency decreased CYP2C11-mediated testosterone 2α- and 16α-hydroxylase activities by 43 and 42%, respectively, whereas severe zinc deficiency reduced each of these activities by approximately 60%. The decrease in CYP2C11 activity was accompanied by a reduction in CYP2C11 protein and mRNA levels, as assessed by immunoblot and reverse transcription-polymerase chain reaction (RT-PCR) assays, respectively. Additional RT-PCR analysis indicated that severe zinc deficiency decreased CYP3A2 and CYP3A18 mRNA levels by 49 and 43%, respectively, whereas it increased CYP2C12 (253%) and CYP3A9 (238%) mRNA expression. Plasma testosterone concentration was decreased by 67% in the marginal zinc-deficient group when compared with the corresponding pair-fed control group. By comparison, it was below the limit of quantification (0.2 ng/mL) in the severe zinc-deficient rats. Overall, these results indicate that dietary zinc deficiency during the developmental period feminized the hepatic gene expression of the sexually dimorphic CYP2C11, CYP3A2, CYP3A18, CYP2C12, and CYP3A9 in postpubertal male rats.

Zinc deficiency reduces leptin gene expression and leptin secretion in rat adipocytes.

The present study was conducted to measure ob mRNA abundance in the zinc-deficient (ZD) rats and the secretion of leptin from adipose tissue obtained from ZD, zinc-adequate (ZA), and pair-fed (PF) rats. It was found that ob mRNA abundance was greatest (P < 0.05) in adipose tissue obtained from ZA and PF rats. Ob mRNA abundance was similar in PF and ZD rats. To study leptin secretion from adipose tissue in a cell culture model, a method was developed to use excised epididymal adipose tissue from ZD, ZA, and PF rats. Tissue was incubated in Opti-modified Eagle's medium (MEM) cell culture medium in which concentrations of zinc and insulin were manipulated. It was observed that leptin secretion was higher (P < 0.05) in adipose tissue obtained from ZA than ZD and PF rats. Secretion of leptin was higher in adipose tissue of PF than ZD rats (P < 0.05). Surprisingly, media zinc content in this ex vivo model tended to suppress secretion of leptin. This suppression seems to be zinc specific and might be caused by the sequestration of insulin in the culture medium. Our results indicate that the reduction in serum leptin observed in ZD rats is likely caused by not only a reduction in body fat, but also by a decrease in leptin synthesis and secretion per gram of adipose tissue. Taking these results into account along with a prior study (1), it is possible that even a marginal zinc deficiency could affect leptin secretion and serum leptin concentrations. Impaired leptin secretion caused by zinc deficiency might be one factor contributing to hypogonadism observed in zinc deficiency.

Immunobiology of gestational zinc deficiency

The trace element zinc is an essential micronutrient for the proper functioning of the immune system. Zinc deficiency leads to impaired function of the unspecific and specific immune response and consequently to an increased susceptibility to bacterial, viral and fungal infections. Immunological defects are not only seen in pronounced but even in marginal and moderate zinc deficiency. Lack of zinc is especially harmful for the development of the immune system, which stresses the importance of a balanced zinc level during pregnancy. However, gestational zinc deficiency due to an imbalance between intake and increased requirements is a common problem world-wide. In animals, gestational zinc deficiency results in reduced thymic and spleen size and depressed active and passive immunity in the infant. For example, depressed immunoglobulin levels, altered antibody repertoire, reduced proliferative response of lymphocytes and diminished neutrophil functions have been reported. Interestingly, immune defects caused by prenatal zinc deficiency, such as depressed antibody levels and lymphocyte proliferation, may even persist in subsequent generations and are not reversible by postnatal zinc administration. Since gestational zinc deficiency is a common problem throughout all cultures and socioeconomic levels, it might have immense consequences for the health status of the population. Based on a summary of the immunobiology of zinc, this article reviews the significance of zinc deficiency during pregnancy and the effect of gestational zinc deficiency on passive and active immunity in the infant. It provides a rational basis for both immunological laboratory investigations and field studies, such as large community-based zinc supplementation trials in pregnant women.

Immunobiology of gestational zinc deficiency

The trace element zinc is an essential micronutrient for the proper functioning of the immune system. Zinc deficiency leads to impaired function of the unspecific and specific immune response and consequently to an increased susceptibility to bacterial, viral and fungal infections. Immunological defects are not only seen in pronounced but even in marginal and moderate zinc deficiency. Lack of zinc is especially harmful for the development of the immune system, which stresses the importance of a balanced zinc level during pregnancy. However, gestational zinc deficiency due to an imbalance between intake and increased requirements is a common problem world-wide. In animals, gestational zinc deficiency results in reduced thymic and spleen size and depressed active and passive immunity in the infant. For example, depressed immunoglobulin levels, altered antibody repertoire, reduced proliferative response of lymphocytes and diminished neutrophil functions have been reported. Interestingly, immune defects caused by prenatal zinc deficiency, such as depressed antibody levels and lymphocyte proliferation, may even persist in subsequent generations and are not reversible by postnatal zinc administration. Since gestational zinc deficiency is a common problem throughout all cultures and socioeconomic levels, it might have immense consequences for the health status of the population. Based on a summary of the immunobiology of zinc, this article reviews the significance of zinc deficiency during pregnancy and the effect of gestational zinc deficiency on passive and active immunity in the infant. It provides a rational basis for both immunological laboratory investigations and field studies, such as large community-based zinc supplementation trials in pregnant women.

Effect of dietary zinc intake on N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats.

Numerous studies have shown that zinc nutrition influences the growth of several types of tumor. However, the influence of zinc nutrition on mammary tumorigenesis is not known. To study the effects of dietary zinc intake on N-methyl-N-nitrosourea (MNU)-induced mammary tumorigenesis, female Sprague-Dawley rats were fed an egg-white-based diet providing 3 (Z3), 12 (Z12), or 31 (Z31) mg zinc/kg diet ad libitum. In addition, two pair-fed controls, PFZ12 and PFZ31, were also included. Fourteen weeks after MNU injection, cumulative tumor incidence and total number of tumors were lower in Z3 rats than in Z12 and Z31 rats. Cumulative tumor incidence and total number of tumors were lower in Z3 rats than in PFZ12 rats, but were the same as in PFZ31 rats. Cumulative tumor incidence and total number of tumors were also lower in pair-fed controls than in their corresponding ad libitum controls, but were the same between the ad libitum controls. Overall, the results showed that the effect of marginal zinc deficiency on MNU-induced mammary tumorigenesis in rats was primarily the result of a reduced feed intake associated with marginal zinc deficiency rather than zinc per se.

Dietary Factors Influencing Zinc Absorption

Marginal zinc deficiency and suboptimal zinc status have been recognized in many groups of the population in both less developed and industrialized countries. Although the cause in some cases may be inadequate dietary intake of zinc, inhibitors of zinc absorption are most likely the most common causative factor. Phytate, which is present in staple foods like cereals, corn and rice, has a strong negative effect on zinc absorption from composite meals. Inositol hexaphosphates and pentaphosphates are the phytate forms that exert these negative effects, whereas the lower phosphates have no or little effect on zinc absorption. The removal or reduction of phytate by enzyme (phytase) treatment, precipitation methods, germination, fermentation or plant breeding/genetic engineering markedly improves zinc absorption. Iron can have a negative effect on zinc absorption, if given together in a supplement, whereas no effect is observed when the same amounts are present in a meal as fortificants. Cadmium, which is increasing in the environment, also inhibits zinc absorption. The amount of protein in a meal has a positive effect on zinc absorption, but individual proteins may act differently; e.g., casein has a modest inhibitory effect of zinc absorption compared with other protein sources. Amino acids, such as histidine and methionine, and other low-molecular-weight ions, such as EDTA and organic acids (e.g., citrate), are known to have a positive effect on zinc absorption and have been used for zinc supplements. Knowledge about dietary factors that inhibit zinc absorption and about ways to overcome or remove these factors is essential when designing strategies to improve the zinc nutrition of vulnerable groups.

Assessment of Marginal Zinc Status in Humans

The assessment of marginal zinc status is problematic. Currently, there is no universally accepted single measure to assess zinc status in humans. The development of a reliable measure of marginal or moderate zinc status would be useful for a variety of purposes. For example, a simple, yet sensitive and accurate measure of zinc nutritional status is critically needed to further our limited understanding of the possible associations between zinc status and the risk of developing various chronic diseases and in predicting favorable health outcomes in patient populations. A convenient and reliable zinc assessment tool is needed to identify subpopulations who are at a risk of zinc deficiency and as an objective guidepost to determine the need for initiation of zinc supplementation or zinc fortification of the food supply, as well in the refinement of recommendations of dietary zinc allowances. In frank zinc deficiency, clinical signs and static measures of zinc concentrations in a variety of readily available tissues, such as plasma, various blood cell types and hair, may uniformly confirm the presence of depleted body zinc stores. However, in general, the relative insensitivity or imprecision of these measurements has resulted in general disappointment in their use to assess marginal zinc status. Therefore, the search continues to find a useful and reliable marker of marginal zinc deficiency. In an attempt to speculate on possible future developments in the zinc status assessment field, a number of new and potentially promising approaches to this problem are highlighted.

Zinc deficiency and taste dysfunction; contribution of carbonic anhydrase, a zinc-metalloenzyme, to normal taste sensation.

The present study was designed to clarify the effect of zinc deficiency on sodium chloride preference, the lingual trigeminal and taste nerves transduction, and carbonic anhydrase (CA) activity of the tongue surface and salivary gland. Male SD rats, 4 weeks old, were divided into four groups, and fed zinc-deficient (Zn-Def), low-zinc (Low-Zn), and zinc-sufficient diets with free access (Zn-Suf) and pair-feeding (Pair-fed). After taking part in the preference tests for 42 days, the rats were provided for the chorda tympani and lingual trigeminal nerves recordings, then finally sacrificed and the tongue and submandibular gland excised to measure CA activity. Sodium chloride preference increased only after 4 days of the feeding of zinc-deficient and low-zinc diets, which means that the taste abnormality appears abruptly in zinc deficieny and even though in marginal zinc deficiency. Reduced CA activities of the taste-related tissues in zinc-deficient group paralleled well with the decreased taste and lingual trigeminal nerves sensitivities.