The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
Agnes Michalczyk - One of the best experts on this subject based on the ideXlab platform.
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Zinc Deficiency and its inherited disorders a review
Genes and Nutrition, 2006Co-Authors: Leigh M Ackland, Agnes MichalczykAbstract:Zinc is an essential trace element required by all living organisms because of its critical roles both as a structural component of proteins and as a cofactor in enzyme catalysis. The importance of Zinc in human metabolism is illustrated by the effects of Zinc Deficiency, which include a diminished immune response, reduced healing and neurological disorders. Furthermore, nutritional Zinc Deficiency can be fatal in newborn or growing animals. While Zinc Deficiency is commonly caused by dietary factors, several inherited defects of Zinc Deficiency have been identified. Acrodermatitis enteropathica is the most commonly described inherited condition found in humans. In several of the few cases that have been reported, this disorder is associated with mutations in the hZIP4 gene, a member of the SLC39 family, whose members encode membranebound putative Zinc transporters. Mutations in other members of this family or in different genes may account for other cases of acrodermatitis in which defects in hZIP4 have not been detected. Another inherited form of Zinc Deficiency occurs in the lethal milk mouse, where a mutation in ZnT4 gene, a member of the SLC30 family of transmembrane proteins results in impaired secretion of Zinc into milk from the mammary gland. A similar disorder to the lethal milk mouse occurs in humans. In the few cases studied, no changes in ZnT4 orthologue, hZnT4, were detected. This, and the presence of several minor phenotypic differences between the Zinc Deficiency in humans and mice, suggests that the human condition is caused by defects in genes that are yet to be identified. Taking into account the fact that there are no definitive tests for Zinc Deficiency and that this disorder can go undiagnosed, plus the recent identification of multiple members of the SCL30 and SLC39, it is likely that mutations in other genes may underlie additional inherited disorders of Zinc Deficiency.
Zhanxiang Zhou - One of the best experts on this subject based on the ideXlab platform.
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dietary Zinc Deficiency exaggerates ethanol induced liver injury in mice involvement of intrahepatic and extrahepatic factors
PLOS ONE, 2013Co-Authors: Wei Zhong, Craig J. Mcclain, Yantao Zhao, Zhenyuan Song, Zhanxiang ZhouAbstract:Clinical studies have demonstrated that alcoholics have a lower dietary Zinc intake compared to health controls. The present study was undertaken to determine the interaction between dietary Zinc Deficiency and ethanol consumption in the pathogenesis of alcoholic liver disease. C57BL/6N mice were subjected to 8-week feeding of 4 experimental liquid diets: (1) Zinc adequate diet, (2) Zinc adequate diet plus ethanol, (3) Zinc deficient diet, and (4) Zinc deficient diet plus ethanol. Ethanol exposure with adequate dietary Zinc resulted in liver damage as indicated by elevated plasma alanine aminotransferase level and increased hepatic lipid accumulation and inflammatory cell infiltration. Dietary Zinc Deficiency alone increased hepatic lipid contents, but did not induce hepatic inflammation. Dietary Zinc Deficiency showed synergistic effects on ethanol-induced liver damage. Dietary Zinc Deficiency exaggerated ethanol effects on hepatic genes related to lipid metabolism and inflammatory response. Dietary Zinc Deficiency worsened ethanol-induced imbalance between hepatic pro-oxidant and antioxidant enzymes and hepatic expression of cell death receptors. Dietary Zinc Deficiency exaggerated ethanol-induced reduction of plasma leptin, although it did not affect ethanol-induced reduction of white adipose tissue mass. Dietary Zinc Deficiency also deteriorated ethanol-induced gut permeability increase and plasma endotoxin elevation. These results demonstrate, for the first time, that dietary Zinc Deficiency is a risk factor in alcoholic liver disease, and multiple intrahepatic and extrahepatic factors may mediate the detrimental effects of Zinc Deficiency.
Leigh M Ackland - One of the best experts on this subject based on the ideXlab platform.
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Zinc Deficiency and its inherited disorders a review
Genes and Nutrition, 2006Co-Authors: Leigh M Ackland, Agnes MichalczykAbstract:Zinc is an essential trace element required by all living organisms because of its critical roles both as a structural component of proteins and as a cofactor in enzyme catalysis. The importance of Zinc in human metabolism is illustrated by the effects of Zinc Deficiency, which include a diminished immune response, reduced healing and neurological disorders. Furthermore, nutritional Zinc Deficiency can be fatal in newborn or growing animals. While Zinc Deficiency is commonly caused by dietary factors, several inherited defects of Zinc Deficiency have been identified. Acrodermatitis enteropathica is the most commonly described inherited condition found in humans. In several of the few cases that have been reported, this disorder is associated with mutations in the hZIP4 gene, a member of the SLC39 family, whose members encode membranebound putative Zinc transporters. Mutations in other members of this family or in different genes may account for other cases of acrodermatitis in which defects in hZIP4 have not been detected. Another inherited form of Zinc Deficiency occurs in the lethal milk mouse, where a mutation in ZnT4 gene, a member of the SLC30 family of transmembrane proteins results in impaired secretion of Zinc into milk from the mammary gland. A similar disorder to the lethal milk mouse occurs in humans. In the few cases studied, no changes in ZnT4 orthologue, hZnT4, were detected. This, and the presence of several minor phenotypic differences between the Zinc Deficiency in humans and mice, suggests that the human condition is caused by defects in genes that are yet to be identified. Taking into account the fact that there are no definitive tests for Zinc Deficiency and that this disorder can go undiagnosed, plus the recent identification of multiple members of the SCL30 and SLC39, it is likely that mutations in other genes may underlie additional inherited disorders of Zinc Deficiency.
Ananda S. Prasad - One of the best experts on this subject based on the ideXlab platform.
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Zinc Deficiency and the Eye
Handbook of Nutrition Diet and the Eye, 2014Co-Authors: Benjamin P. Nicholson, Ananda S. Prasad, Emily Y. ChewAbstract:Abstract In the syndrome of iron-Deficiency anemia, hepatosplenomegaly, dwarfism, and hypogonadism, Zinc Deficiency accounts for dwarfism and hypogonadism and the anemia is due to iron Deficiency. The ocular manifestations of Zinc Deficiency in humans include impaired dark adaptation and nyctalopia. The mechanism of retinal dysfunction in Zinc Deficiency is not well understood, although several mechanisms have been proposed. The results of the Age-Related Eye Disease Study (AREDS) demonstrate a role for the specific AREDS antioxidant with Zinc formulation for the prevention of advanced age-related macular degeneration (AMD). The AREDS formulation is recommended as a treatment for nonsmokers with extensive intermediate drusen, large drusen, noncentral geographic atrophy, or unilateral advanced AMD. AREDS2 is an ongoing study of supplements for patients at risk of vision loss due to AMD, and it will compare a lower Zinc dose (25 mg) with the current AREDS dose (80 mg). Severe Zinc Deficiency, particularly in the form of acrodermatitis enteropathica, is associated with ocular surface disease. Randomized trials of Zinc supplementation have not shown a clear benefit for cataract.
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effects of Zinc Deficiency on th1 and th2 cytokine shifts
The Journal of Infectious Diseases, 2000Co-Authors: Ananda S. PrasadAbstract:Nutritional Deficiency of Zinc is widespread throughout developing countries, and Zinc-deficient persons have increased susceptibility to a variety of pathogens. Zinc Deficiency in an experimental human model caused an imbalance between Th1 and Th2 functions. Production of interferon-gamma and interleukin (IL)-2 (products of Th1) were decreased, whereas production of IL-4, IL-6, and IL-10 (products of Th2) were not affected during Zinc Deficiency. Zinc Deficiency decreased natural killer cell lytic activity and percentage of precursors of cytolytic T cells. In HuT-78, a Th0 cell line, Zinc Deficiency decreased gene expression of thymidine kinase, delayed cell cycle, and decreased cell growth. Gene expression of IL-2 and IL-2 receptors (both alpha and beta) and binding of NF-kappaB to DNA were decreased by Zinc Deficiency in HuT-78. Decreased production of IL-2 in Zinc Deficiency may be due to decreased activation of NF-kappaB and subsequent decreased gene expression of IL-2 and IL-2 receptors.
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Effects of Zinc Deficiency on immune functions
Journal of Trace Elements in Experimental Medicine, 2000Co-Authors: Ananda S. PrasadAbstract:Nutritional Deficiency of Zinc is widespread throughout the developing world. Zinc deficient subjects experience increased susceptibility to a variety of infections. Zinc Deficiency in an experimental human model caused an imbalance between Th1 and Th2 functions. Production of IFN-γ and IL-2 (products of TH1) were decreased, whereas production of IL-4, IL-6 and IL-10 (products of Th2) were not affected due to Zinc Deficiency. Zinc Deficiency decreased NK cell lytic activity and percentage of precursors of cytolytic T cells. In HUT-78, a Th0 cell line, Zinc Deficiency decreased gene expression of deoxythymidine kinase (TK), delayed cell cycle and decreased cell growth. Gene expression of IL-2 and IL-2 receptors (both α and β) and binding of NF-kB to DNA were decreased by Zinc Deficiency in HUT-78. In HL-60, a monocytic-macrophage cell line, Zinc Deficiency increased production and gene expression of TNF-α, IL-1β and IL-8. These cytotoxic cytokines are known to produce increased free radicals. Thus Zinc may function as an important anti-oxidant. In conclusion, decreased production of IL-2 in Zinc Deficiency may be due to decreased activation of NF-kB and subsequent decreased gene expression of IL-2 and IL-2 receptor α. Our studies show that Zinc Deficiency affects cell-mediated immunity and leads to activation of monocytes-macrophages and may play an important role as an antioxidant. J. Trace Elem. Exp. Med. 13:1–20, 2000. © 2000 Wiley-Liss, Inc.
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Clinical Spectrum of Human Zinc Deficiency
Biochemistry of Zinc, 1993Co-Authors: Ananda S. PrasadAbstract:During the past two decades, a spectrum of clinical Deficiency of Zinc in human subjects has been recognized. At one end, the manifestations of Zinc Deficiency may be severe, and at the other end, Zinc Deficiency may be mild or marginal.
Toyoharu Tsutsui - One of the best experts on this subject based on the ideXlab platform.
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Infants and elderlies are susceptible to Zinc Deficiency.
Scientific Reports, 2016Co-Authors: Hiroshi Yasuda, Toyoharu TsutsuiAbstract:The importance of Zinc for human health has been recognized since the early 1960s, but today there is little concern about Zinc Deficiency in developed countries. In this study, we measured the Zinc concentration in hair from 28,424 Japanese subjects (18,812 females and 9,612 males) and found that 1,754 subjects (6.17%) had Zinc concentrations lower than 2 standard deviations (86.3 ppm) below the control reference range, which qualifies as Zinc Deficiency. In particular, a considerable proportion of elderlies and children (20% or more) were found to have marginal to severe Zinc Deficiency. A Zinc concentration of 9.7 ppm was the lowest observed in a 51-year-old woman; this concentration was approximately 1/13 of the mean reference level. The prevalence of Zinc Deficiency in adults increased with aging to a maximum of 19.7% by the 8th decade of life and decreased to 3.4% above 90-year-old. The proportion of Zinc Deficiency in infants 0–4 years was 36.5% in males and 47.3% in females; these percentages were higher than the maximum prevalence in elderly subjects. These findings suggest that infants and elderlies are prone to Zinc Deficiency and that intervention of Zinc Deficiency is necessary for normal human development, health and longevity.
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infantile Zinc Deficiency association with autism spectrum disorders
Scientific Reports, 2011Co-Authors: Hiroshi Yasuda, Kazuya Yoshida, Yuichi Yasuda, Toyoharu TsutsuiAbstract:Elucidation of the pathogenesis and effective treatment of autism spectrum disorders is one of the challenges today. In this study, we examine hair Zinc concentrations for 1,967 children with autistic disorders (1,553 males and 414 females), and show considerable association with Zinc Deficiency. Histogram of hair Zinc concentration was non-symmetric with tailing in lower range, and 584 subjects were found to have lower Zinc concentrations than -2 standard deviation level of its reference range (86.3-193 ppm). The incidence rate of Zinc Deficiency in infant group aged 0-3 year-old was estimated 43.5 % in male and 52.5 % in female. The lowest Zinc concentration of 10.7 ppm was detected in a 2-year-old boy, corresponding to about 1/12 of the control mean level. These findings suggest that infantile Zinc Deficiency may epigenetically contribute to the pathogenesis of autism and nutritional approach may yield a novel hope for its treatment and prevention.
