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Dietary Minerals and Metabolic Disorders

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (20 February 2023) | Viewed by 2944

Special Issue Editor


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Guest Editor
Department of Human Nutrition and Dietetics, Poznan University of Life Sciences, Poznan, Poland
Interests: the influence of pharmacological and nutritional factors on mineral status; drug-food-supplements interactions; the assessment of mineral balance in women depending on the physiological state and age; the relationship between the concentration of essential and toxic elements in the amniotic fluid and blood serum and the development of the fetus as well as the study of nutritional and health factors influencing the mineral balance of pregnant women

Special Issue Information

Dear Colleagues,

Minerals are involved in many physiological processes in the body and their deficiency or excess may lead to metabolic disorders and the development of many diseases. An adequate supply of minerals ensures proper nutritional status, and proper mineral status is important during the entirity of life, but especially in prenatal life. There are many nutritional and non-nutritional factors that may affect mineral status, including diet, supplements, pharmacological treatment, and environmental factors. Mineral status depends on the process of absorption and factors that affect their bioavailability. Interactions between minerals and nutrients and also other factors play an important role in the effectiveness of absorption and influence mineral metabolism and physiological process.

This Special Issue focuses mainly on the association between mineral intake and metabolic diseases. This cycle also includes the problems of deficiency and excess minerals, the determining the factors affecting the bioavailability of minerals and their relationship with the nutritional status and health, and the use of mineral supplements in terms of positive effects and side effects on the organism.

This Special Issue of Nutrients entitled “Dietary Minerals and Metabolic Disorders” welcomes original research and reviews of the literature concerning this important topic.

Dr. Joanna Suliburska
Guest Editor

Manuscript Submission Information

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Keywords

  • minerals
  • diet
  • bioavailability
  • deficiency
  • supplements
  • metabolic disorders

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Published Papers (1 paper)

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Research

13 pages, 3941 KiB  
Article
Depletion of Zinc Causes Osteoblast Apoptosis with Elevation of Leptin Secretion and Phosphorylation of JAK2/STAT3
by Jennifer K. Lee, Jung-Heun Ha, Do-Kyun Kim, JaeHee Kwon, Young-Eun Cho and In-Sook Kwun
Nutrients 2023, 15(1), 77; https://doi.org/10.3390/nu15010077 - 23 Dec 2022
Cited by 5 | Viewed by 2397
Abstract
Zinc (Zn) has been reported to mediate leptin secretion, and thus leptin can be an important candidate molecule linking Zn with bone formation. The present study investigated whether zinc deficiency induces leptin secretion by activating a JAK2/STAT3 signaling pathway and leads to osteoblastic [...] Read more.
Zinc (Zn) has been reported to mediate leptin secretion, and thus leptin can be an important candidate molecule linking Zn with bone formation. The present study investigated whether zinc deficiency induces leptin secretion by activating a JAK2/STAT3 signaling pathway and leads to osteoblastic apoptosis. MC3T3-E1 cells were incubated for 24 h in normal osteogenic differentiation medium (OSM) or OSM treated with either 1 μM (Low Zn) or 15 μM (High Zn) of ZnCl2 containing 5 μM TPEN (Zn chelator). Our results demonstrated that low Zn stimulated extracellular leptin secretion and increased mRNA and protein expression of leptin in osteoblastic MC3T3-E1 cells. The OB-Rb (long isoform of leptin receptor) expressions were also elevated in osteoblasts under depletion of Zn. Leptin-signaling proteins, JAK2 and p-JAK2 in the cytosol of low Zn osteoblast conveyed leptin signaling, which ultimately induced higher p-STAT3 expression in the nucleus. Apoptotic effects of JAK2/STAT3 pathway were shown by increased caspase-3 in low Zn osteoblasts as well as apoptotic morphological features observed by TEM. Together, these data suggest that low Zn modulates leptin secretion by activating JAK2/STAT3 signaling pathway and induces apoptosis of osteoblastic MC3T3-E1 cells. Full article
(This article belongs to the Special Issue Dietary Minerals and Metabolic Disorders)
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