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Zinc Deficiency and Supplementation Related to Metabolic Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Micronutrients and Human Health".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 1692

Special Issue Editor

Department of Nutritional Sciences & Toxicology, University of California, Berkeley, CA 94720, USA
Interests: calcium; zinc; pregnancy; lactation; aging; insufficient; excessive intakes

Special Issue Information

Dear Colleagues,

Zinc, like iron and copper, is a trace element that is essential for numerous metabolic processes. These elements are referred to as trace elements because the daily requirement to support growth, development, and physiological functions is less than 100 mg/d. 

Zinc, the most ubiquitous trace element, is present throughout all biologic systems, where it has abundant, varied functions. More than 100 enzymes require zinc to perform catalytic functions. It participates in all major biochemical pathways, and it plays multiple roles in the perpetuation of genetic material, i.e., DNA transcription, RNA translation, and cellular division.   Given the diverse array of zinc-dependent biological functions, it is not surprising that the zinc status of an individual influences multiple metabolic functions i.e., growth, immune competence, and neuro-behavioral development. Although zinc deficiency is one of the most common nutrient deficiencies worldwide, the broad range of physiological signs of zinc deficiency make it difficult to identify. Nevertheless, the likelihood of zinc deficiency in a population can be assessed by reviewing the adequacy of zinc in the food supply and the rate of stunting in preschool children.

Dr. Janet King
Guest Editor

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Keywords

  • zinc
  • food sources
  • tissue distribution
  • growth
  • immune function
  • endocrine function
  • reproduction

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Published Papers (1 paper)

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Research

15 pages, 4505 KiB  
Article
Zinc Deficiency Promotes Calcification in Vascular Smooth Muscle Cells Independent of Alkaline Phosphatase Action and Partly Impacted by Pit1 Upregulation
by Ethel H. Alcantara, Jae-Hee Kwon, Min-Kyung Kang, Young-Eun Cho and In-Sook Kwun
Nutrients 2024, 16(2), 291; https://doi.org/10.3390/nu16020291 - 18 Jan 2024
Cited by 2 | Viewed by 1408
Abstract
Inorganic phosphate (Pi) is a critical determinant of calcification, and its concentration is regulated by alkaline phosphatase (ALP) and Pit1. ALP is a key regulator of osteogenic calcification and acts by modulating local inorganic phosphate (Pi) concentrations through hydrolyzing pyrophosphate in the extracellular [...] Read more.
Inorganic phosphate (Pi) is a critical determinant of calcification, and its concentration is regulated by alkaline phosphatase (ALP) and Pit1. ALP is a key regulator of osteogenic calcification and acts by modulating local inorganic phosphate (Pi) concentrations through hydrolyzing pyrophosphate in the extracellular matrix (ECM). Pit1, a sodium-dependent phosphate transporter, regulates calcification via facilitating phosphate uptake within the cells. To investigate whether zinc differentially regulates osteoblastic and vascular calcifications, we examined ALP activity and Pit1 in osteoblastic and vascular smooth muscle cells (VSMCs). Our findings demonstrate that calcification in osteoblastic MC3T3-E1 cells is decreased via diminished ALP action under zinc deficiency. In contrast, zinc-deficiency-induced calcification in VSMCs is independent of ALP action, as demonstrated by very weak ALP activity and expression in calcified VSMCs. In zinc-deficient A7r5 VSMC, P accumulation increased with increasing Na phosphate concentration (3–7 mM) but not with β-GP treatment, which requires ALP activity to generate Pi. Ca deposition also increased with Na phosphate in a dose-dependent manner; in contrast, β-GP did not affect Ca deposition. In osteoblastic cells, Pit1 expression was not affected by zinc treatments. In contrast, Pit1 expression is highly upregulated in A7r5 VSMC under zinc deficiency. Using phosphonoformic acid, a competitive inhibitor of Pit1, we showed that calcification is inhibited in both A7r5 and MC3T3-E1 cells, indicating a requirement for Pit1 in both calcifications. Moreover, the downregulation of VSMC markers under zinc deficiency was restored by blocking Pit1. Taken together, our results imply that zinc-deficiency-induced calcification in VSMC is independent of ALP action in contrast to osteoblastic calcification. Moreover, Pit1 expression in VSMCs is a target for zinc deficiency and may mediate the inhibition of VSMC marker expression under zinc deficiency. Full article
(This article belongs to the Special Issue Zinc Deficiency and Supplementation Related to Metabolic Diseases)
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