Special Issue "Zinc in Health and Disease"
Quicklinks
A special issue of Nutrients (ISSN 2072-6643).
Deadline for manuscript submissions: closed (30 April 2012)
Special Issue Editors
Guest Editor
Dr. Samir Samman
Discipline of Nutrition & Metabolism, Room 475, School of Molecular & Microbial Biosciences, G08 University of Sydney, NSW, Australia
Website: http://sydney.edu.au/science/molecular_bioscience/people/profiles/ssamman.php
E-Mail: samir.samman@sydney.edu.au
Phone: +61 2 9351 2476 / 9351 6022
Interests: human nutrition and health with research projects in the areas of diet and heart disease and nutrient requirements; nutraceuticals and environmental nutrition
Guest Editor
Dr. Nicola Lowe
International Institute of Nutritional Sciences, University of Central Lancashire, Lancashire, PR1 2HE, UK
Website: http://www.uclan.ac.uk/schools/ssto/about_the_school/sport/cases/nicola_lowe.php
E-Mail: NMLowe@uclan.ac.uk
Phone: +44 1772 893599
Interests: micronutrient requirements, with a particular interest in Zinc requirements and metabolism
Guest Editor
Dr. Arthur Grider
Department of Foods and Nutrition, The University of Georgia, Athens, GA 30602, USA
Website: http://fcs.uga.edu/fdn/faculty.php?id=138
E-Mail: agrider@fcs.uga.edu
Phone: +1 706 542 7371
Fax: +1 706 542 5059
Interests: Cellular and tissue zinc metabolism; proteomic analysis of biological samples; nutritional biomarkers; plant polyphenol metabolism
Special Issue Information
Dear Colleagues,
Zinc contributes to the proper functioning of numerous enzymes, the structural integrity of cellular components, and regulation of gene expression. Zinc is widely distributed in foods, and its bioavailability is affected by other dietary constituents. Regulation of zinc metabolism is achieved through a balance of absorption and excretion and involves adaptive mechanisms. Zinc ions influence a number of signal transduction pathways, including insulin signaling, and regulate leptin secretion from adipose tissue, potentially linking cellular zinc metabolism to apoptosis, insulin resistance and dyslipidemia. The aim of this focus issue is to explore zinc bioavailability, biomarkers of zinc status, and the relationships between zinc intake and chronic disease.
Dr. Samir Samman
Dr. Nicola Lowe
Dr. Arthur Grider
Guest Editors
Submission
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs).
Keywords
- zinc
- diet
- supplements
- bioavailability
- biomarkers
- status
- diabetes
- cardiovascular disease
- inflammation
- cognitive function
Published Papers (8 papers)
|
Received: 17 April 2012; in revised form: 17 May 2012 / Accepted: 29 May 2012 / Published: 6 June 2012
Show/Hide Abstract
| Download PDF Full-text (203 KB) | Download XML Full-text
Abstract: Zinc deficiency is one of the leading risk factors for developing disease and yet we do not have a clear understanding of the mechanisms behind the increased susceptibility to infection. This review will examine the interrelationships among the hypothalamus-pituitary-adrenal stress axis, p56lck, and T-cell maturation in both zinc deficiency and responses during zinc repletion. We will highlight differences between the adult mouse model (wasting malnutrition) and growing rat model (stunting malnutrition) of dietary zinc deficiency and discuss the use of various controls to separate out the effects of zinc deficiency from the associated malnutrition. Elevated serum corticosterone in both zinc deficient and pair-fed rats does not support the hypothesis that zinc deficiency per se leads to corticosterone-induced apoptosis and lymphopenia. In fact, the zinc deficient rat does not have lymphopenia. Thymocytes from zinc deficient mice and rats have elevated levels of p56lck, a signalling protein with a zinc clasp structure, but this does not appear to affect thymocyte maturation. However, post-thymic T-cell maturation appears to be altered based on the lower proportion of splenic late thymic emigrants in zinc deficient rats. Fewer new T-cells in the periphery could adversely affect the T-cell repertoire and contribute to immunodeficiency in zinc deficiency.
|
|
Received: 4 May 2012; in revised form: 4 June 2012 / Accepted: 11 June 2012 / Published: 14 June 2012
Show/Hide Abstract
| Download PDF Full-text (185 KB) | Download XML Full-text
Abstract: A cross-sectional survey of 2819 adults aged 20 years and above was undertaken in 2002 in Jiangsu Province. Zinc intake was assessed using a consecutive 3-day 24-h dietary recall method. Insufficient and excess intake was determined according to the Chinese Dietary Recommended Intakes. Four distinct dietary patterns were identified namely “traditional”, “macho”, “sweet tooth”, and “healthy”. Intake of zinc from biofortified rice was simulated at an intermediate zinc concentration (2.7 mg/100 g) and a high zinc concentration (3.8 mg/100 g) in rice. Average total zinc intake was 12.0 ± 3.7 mg/day, and insufficiency of zinc intake was present in 15.4%. Simulated zinc intake from biofortified rice with intermediate and high zinc concentration decreased the prevalence of low zinc intake to 6.5% and 4.4%, respectively. The effect was most pronounced in the “traditional” pattern, with only 0.7% of insufficiency of zinc intake remaining in the highest quartile of the pattern. Zinc intake was inversely associated with the “sweet tooth” pattern. Zinc biofortifed rice improves dietary zinc intake and lowers risk for insufficient zinc intake, especially for subjects with a more “traditional” food pattern, but less for subjects with a “sweet tooth” food pattern.
|
|
Received: 7 May 2012; in revised form: 19 June 2012 / Accepted: 20 June 2012 / Published: 26 June 2012
Show/Hide Abstract
| Download PDF Full-text (222 KB) | Download XML Full-text
Abstract: The current Australian Nutrient Reference Values (NRV) use different Estimated Average Requirements (EAR) for zinc for adolescent boys and girls compared to the previous recommendations. The adequacy of zinc intakes of 2–16 years old children (n = 4834) was examined in the 2007 Australian National Children’s Nutrition and Physical Activity Survey. Zinc intakes were estimated from two 24-h recalls and compared with age- and gender-specific NRV. Food sources of zinc were assessed and compared with those of the 1995 National Nutrition Survey. The mean (SD) zinc intake was 10.2 (3.0) mg/day for all children. Nearly all children met the EAR for zinc except for 14–16 years old boys (29% did not meet EAR). Children (2–3 years) were at highest risk of excessive zinc intakes with 79% exceeding the Upper Level of Intake. Meat and poultry; milk products; and cereals and cereal products contributed 68% of total zinc intake. The contribution of cereals to total zinc intake has increased significantly since 1995, due to the greater market-availability of zinc-fortified breakfast cereals. We conclude that sub-groups of Australian children are at-risk of inadequate (boys 14–16 years) or excessive (children 2–3 years) zinc intakes, and monitoring of zinc status is required.
|
|
Received: 3 May 2012; in revised form: 7 June 2012 / Accepted: 27 June 2012 / Published: 4 July 2012
Show/Hide Abstract
| Download PDF Full-text (240 KB) | Download XML Full-text
Abstract: Zinc is a trace mineral which is vital for the functioning of numerous cellular processes, is critical for growth, and may play an important role in cancer etiology and outcome. The intracellular levels of this mineral are regulated through the coordinated expression of zinc transporters, which modulate both zinc influx as well as efflux. LIV-1 (ZIP6) was first described in 1988 as an estrogen regulated gene with later work suggesting a role for this transporter in cancer growth and metastasis. Despite evidence of its potential utility as a target gene for cancer prognosis and treatment, LIV-1 has received relatively little attention, with only three prior reviews being published on this topic. Herein, the physiological effects of zinc are reviewed in light of this mineral’s role in cancer growth with specific attention being given to LIV-1 and the potential importance of this transporter to breast cancer etiology.
|
|
Received: 28 April 2012; in revised form: 8 June 2012 / Accepted: 25 June 2012 / Published: 4 July 2012
Show/Hide Abstract
| Download PDF Full-text (270 KB) | Download XML Full-text
Abstract: In atherosclerosis and diabetes mellitus, the concomitant presence of low-grade systemic inflammation and mild zinc deficiency highlights a role for zinc nutrition in the management of chronic disease. This review aims to evaluate the literature that reports on the interactions of zinc and cytokines. In humans, inflammatory cytokines have been shown both to up- and down-regulate the expression of specific cellular zinc transporters in response to an increased demand for zinc in inflammatory conditions. The acute phase response includes a rapid decline in the plasma zinc concentration as a result of the redistribution of zinc into cellular compartments. Zinc deficiency influences the generation of cytokines, including IL-1β, IL-2, IL-6, and TNF-α, and in response to zinc supplementation plasma cytokines exhibit a dose-dependent response. The mechanism of action may reflect the ability of zinc to either induce or inhibit the activation of NF-κB. Confounders in understanding the zinc-cytokine relationship on the basis of in vitro experimentation include methodological issues such as the cell type and the means of activating cells in culture. Impaired zinc homeostasis and chronic inflammation feature prominently in a number of cardiometabolic diseases. Given the high prevalence of zinc deficiency and chronic disease globally, the interplay of zinc and inflammation warrants further examination.
|
|
Received: 2 June 2012; in revised form: 12 July 2012 / Accepted: 13 July 2012 / Published: 24 July 2012
Show/Hide Abstract
| Download PDF Full-text (224 KB) | Download XML Full-text
Abstract: Zinc plays critical roles during embryogenesis, fetal growth, and milk secretion, which increase the zinc need for pregnancy and lactation. Increased needs can be met by increasing the dietary zinc intake, along with making homeostatic adjustments in zinc utilization. Potential homeostatic adjustments include changes in circulating zinc, increased zinc absorption, decreased zinc losses, and changes in whole body zinc kinetics. Although severe zinc deficiency during pregnancy has devastating effects, systematic reviews and meta-analysis of the effect of maternal zinc supplementation on pregnancy outcomes have consistently shown a limited benefit. We hypothesize, therefore, that zinc homeostatic adjustments during pregnancy and lactation improve zinc utilization sufficiently to provide the increased zinc needs in these stages and, therefore, mitigate immediate detrimental effects due to a low zinc intake. The specific questions addressed are the following: How is zinc utilization altered during pregnancy and lactation? Are those homeostatic adjustments influenced by maternal zinc status, dietary zinc, or zinc supplementation? These questions are addressed by critically reviewing results from published human studies on zinc homeostasis during pregnancy and lactation carried out in different populations worldwide.
|
|
Received: 4 May 2012; in revised form: 27 June 2012 / Accepted: 10 July 2012 / Published: 26 July 2012
Show/Hide Abstract
| Download PDF Full-text (302 KB) | Download XML Full-text
Abstract: Recommendations for zinc intake during childhood vary widely across Europe. The EURRECA project attempts to consolidate the basis for the definition of micronutrient requirements, taking into account relationships among intake, status and health outcomes, in order to harmonise these recommendations. Data on zinc intake and biomarkers of zinc status reported in randomised controlled trials (RCTs) can provide estimates of dose-response relationships which may be used for underpinning zinc reference values. This systematic review included all RCTs of apparently healthy children aged 1–17 years published by February 2010 which provided data on zinc intake and biomarkers of zinc status. An intake-status regression coefficient () was calculated for each individual study and calculated the overall pooled and SE () using random effects meta-analysis on a double log scale. The pooled dose-response relationship between zinc intake and zinc status indicated that a doubling of the zinc intake increased the serum/plasma zinc status by 9%. This evidence can be utilised, together with currently used balance studies and repletion/depletion studies, when setting zinc recommendations as a basis for nutrition policies.
|
|
Received: 29 May 2012; in revised form: 11 July 2012 / Accepted: 17 July 2012 / Published: 30 July 2012
Show/Hide Abstract
| Download PDF Full-text (372 KB) | Download XML Full-text
Abstract: Worldwide, breast cancer is the most commonly diagnosed cancer among women and is the leading cause of female cancer deaths. Zinc (Zn) functions as an antioxidant and plays a role in maintaining genomic stability. Zn deficiency results in oxidative DNA damage and increased cancer risk. Studies suggest an inverse association between dietary and plasma Zn levels and the risk for developing breast cancer. In contrast, breast tumor biopsies display significantly higher Zn levels compared with normal tissue. Zn accumulation in tumor tissue also correlates with increased levels of Zn importing proteins. Further, aberrant expression of Zn transporters in tumors correlates with malignancy, suggesting that altered metal homeostasis in the breast could contribute to malignant transformation and the severity of cancer. However, studies have yet to link dysregulated Zn transport and abnormal Zn-dependent functions in breast cancer development. Herein, we summarize studies that address the multi-modal role of Zn dyshomeostasis in breast cancer with respect to the role of Zn in modulating oxidative stress, DNA damage response/repair pathways and cell proliferation/apoptosis, and the relationship to aberrant regulation of Zn transporters. We also compare Zn dysregulation in breast tissue to that of prostate, pancreatic and ovarian cancer where possible.
|
Last update: 20 March 2012
