Zinc deficiency is associated with delayed bone healing, skin fragility, and susceptibility to infection due to immunodepression, therefore it has a significant impact on surgical outcomes. The author first became interested in the mechanism of bone healing in a case where an ankle fracture in a dialysis patient did not heal after three operations, and a zinc wave was later found in electron microscopy and electron probe X-ray microanalysis of frozen sections of the ossified area of the yellow ligament. Subsequently, shoulder injections to a rheumatoid arthritis patient caused pyogenic arthritis, suggesting that low zinc levels in rheumatoid arthritis patients resulted in weak skin and a low skin tenderness threshold. Later analysis showed that patients with zinc levels below 50 μg/dL died early due to infections, suggesting that low zinc levels are also related to poor immunity. Two groups were compared after 2 months and after 6 months of supplementation with 34 mg/day of zinc to examine how much zinc should be supplemented by the time of joint replacement surgery. There was no significant difference in zinc levels in the two groups at 1 month before surgery, but at 7 days before surgery and 3 days after surgery, in the first group zinc levels were significantly lower, skin necrosis occurred in three cases, and skin healing was delayed in four cases. If there is concern about the patient’s preoperative condition, it is recommended that zinc levels be measured and that adequate zinc supplementation be performed before surgery.

Zinc is an essential trace element with various physiological functions; it is a structural, catalytic, and signaling component of proteins. Owing to its wide range of functions, zinc deficiency causes various symptoms, such as taste disorders, dermatitis, hair loss, decreased appetite, growth disorders, and gonad dysfunction. The global prevalence of zinc deficiency is estimated to be about 25%; thus, its prevention is important for human health. Approximately 2–3 g of zinc is present in the adult human body. Systemic zinc homeostasis is regulated by the zinc transporters ZIP4 and ZNT1, which play major roles in regulating the absorption of food-derived zinc, primarily in the duodenum and jejunum. ZIP4 is expressed on the apical membrane of intestinal epithelial cells and allows divalent zinc ions to enter cells from the lumen. Zinc in enterocytes is subsequently transported by ZNT1 on the basolateral membrane into the portal vein, where it binds to albumin and α2-macroglobulin. In turn, zinc regulates the expression of ZIP4 and ZNT1. This review briefly describes the mechanism of dietary zinc absorption, focusing on zinc in foods and the transporters involved in zinc absorption in the intestinal tract. Moreover, we discuss the potential of dietary components to increase the efficiency of zinc absorption in the intestinal tract via zinc transporters and improve zinc nutrition.

Zinc (Zn) is an essential trace element for numerous biological events in mammals. Zn functions as a signaling mediator, leading to the regulation of physiological cell actions and, therefore, has therapeutic potential. Recent breast cancer research has shown that Zn transporters contribute to malignancy processes; thus, elucidating the roles of Zn and Zn transporters in breast cancer may lead to the development of novel strategies for breast cancer diagnosis and therapy. The Zn transporter ZIP6 mediates the acquisition of malignant phenotypes such as hypoxic resistance and epithelial-mesenchymal transition (EMT), which determine breast tumor grade and prognosis. ZIP6 expression contributes to the efficacy of anticancer therapy through Zn-induced autophagy. The maintenance of breast cancer stem-like cells requires Zn modulation through the cooperative function of ZIP6 and ZIP7. These findings suggest that the ZIP6-mediated Zn network is a potent driving force toward malignancy. In this review, we summarize recent progress in understanding the emerging roles of Zn and ZIP6 in the regulation of malignant characteristics related to hypoxic adaptive response, drug therapy, and stemness. We also discuss the possibility and future challenges of innovative breast cancer therapies using ZIP6 and Zn-related molecules.

Zinc (Zn) homeostasis is largely regulated by the liver, at the same time, Zn is necessary for the maintenance of normal liver function. Therefore, Zn deficiency results in the impairment of hepatocyte function, leading to chronic liver injuries such as hepatic inflammation, fibrosis and steatosis. Numerous metabolic abnormalities, including impaired glucose tolerance, dyslipidemia, hepatic encephalopathy, and sarcopenia, are also associated with these chronic liver injuries. Zn supplementation can recover these chronic liver injuries and related metabolic disorders. Recent advances in molecular biological techniques have enabled us to elucidate the putative mechanisms by which chronic liver disorders evoke varieties of metabolic abnormalities derived from Zn deficiency. This review focuses on the most recent discoveries regarding the role of Zn deficiency in chronic liver diseases, including chronic hepatitis, liver cirrhosis, nonalcoholic fatty liver disease, and autoimmune liver diseases. Moreover, we would like to verify Zn supplementation on these chronic liver diseases.

Microglia are resident immune cells of the central nervous system (CNS) that continuously survey the local microenvironment by extending and withdrawing their cellular processes in the resting state. When activated by tissue injury or other signals, microglia retract their processes and transform into an activated amoeboid morphology. These activated cells are known to polarize into M1 pro-inflammatory or M2 anti-inflammatory phenotypes during neuropathological conditions, including stroke, which suggests that this polarization might play a role in the development and progression of brain disorders. Furthermore, zinc homeostasis in the CNS is integral to normal CNS function, such as learning and memory. Although the effects of zinc on microglial activation are not well known, recent studies have demonstrated that zinc affects microglial activation as well as neuronal function. In this review, we discuss in detail the effects of extracellular and intracellular zinc levels on microglial activation and the M1 and M2 microglial phenotypes. Extracellular zinc might act as a novel trigger for the microglial morphological changes via a zinc-induced microglial activation signaling pathway, where intracellular zinc accumulation via Zrt-Irt-like protein 1 is the initial step. Additionally, extracellular zinc might promote the inflammatory M1 phenotype, while increased intracellular free zinc levels in interleukin-4-induced M2a microglia might negatively regulate arginase-1 expression. The zinc-promoted M1 phenotype is involved in post-ischemic cognitive decline and suppression of astrocytic engulfing activity, whereas zinc-modulated arginase-1 expression might regulate the phagocytic activity of M2a microglia.

Zinc is a critical trace element that is important for cellular function in both female and male reproductive organs. Zinc imbalance and/or altered zinc signaling causes multiple disorders in the reproductive process, including oogenesis, spermatogenesis, fertilization, and embryogenesis. Extracellular and intracellular dynamics of zinc ions are regulated by cell-specific transporters, i.e., Zrt-, Irt-related protein (ZIP) or zinc transporter (ZnT), which respectively transport zinc ions in or out of the cytoplasm through biological membranes. The expression and function of these transporters vary among cell types. The elucidation of the mechanisms underlying zinc homeostasis and zinc dynamics in reproductive function will lead to better infertility treatments for humans as well as the improvement of livestock production. In this review, we discuss the essential roles of zinc signaling in the key events in mammalian reproduction, with a focus on the period from gametogenesis to embryonic development.

Zinc is an essential trace element that plays various and pivotal roles in the human body. Therefore, zinc homeostasis is tightly regulated by ion channels and zinc transporters, including the Zrt-Irt-like protein (ZIP) and zinc transporter (ZnT) families. Disrupting this zinc homeostasis often causes zinc deficiency in various diseases (e.g., liver cirrhosis, chronic renal diseases, and inflammatory bowel diseases) and contributes to the underlying pathological conditions. Although the amount of zinc in the serum accounts for only approximately 0.1% of the total zinc in the body, this serum concentration is usually measured and analyzed in these diseases. Measuring the serum concentration is the only way to assess pathological conditions and evaluate the effect of zinc treatment when specific symptoms are not observed. For liver diseases, zinc concentrations decrease with the progression of fibrosis in patients with chronic liver diseases (CLDs); thus, many investigators treat these patients with zinc preparations. Supplementation with zinc for not only a short time but also a long time was effective, and the zinc serum concentration is a useful index for achieving good prognosis. Several studies revealed that it is important to maintain a serum zinc concentration of more than70 µg/dl after zinc supplementation, and a quantity of zinc of approximately 90 mg/day is needed in patients with liver cirrhosis.

Background: COVID-19 is an infectious disease caused by the SARS-CoV-2 virus and causing pandemics around the world. Zinc is an essential trace element and important for maintaining immune function. Serum zinc level has been reported to be low in severe cases of COVID-19.

Patients and methods: Patients who were diagnosed with SARS-CoV-2 infection were requested to be examined by our hospital while waiting at home were included. Medical history was heard, body temperature and blood oxygen saturation was measured, blood was collected, and lung CT examination was performed.

Results: The mean age of 102 patients was 39.7 y/o. There were no cases of fever with a body temperature of 37.5 ℃ or higher. Mean serum zinc level was 79.1μg/dL. Comparing serum zinc levels with healthy individuals by age, the serum zinc levels were significantly lower in COVID-19 cases over 50 y/o. Pneumonia findings was found in 54 cases (52.9%). Patients with pneumonia were significantly older than those without pneumonia (48.3 vs 30.1 y/o). Serum zinc levels were significantly lower in patients with pneumonia than in patients without pneumonia (75.5 vs 83.2 μg/dL). Dysosmia and dysgeusia were seen in 36 cases (35.3%). There were significantly younger ages compared to those without dysosmia and dysgeusia (34.4 vs 42.6 y/o). There was no difference in serum zinc levels depending on the presence of dysosmia or dysgeusia.

Conclusion: Serum zinc levels were involved in the development of SARS-CoV-2 infection and pneumonia. The onset of dysosmia or dysgeusia was not associated with serum zinc levels.

We performed a retrospective study of serum zinc levels and blood nutrient indices with malnutrition admitted to our hospital. The association between zinc levels and the onset of pressure ulcer was then investigated. The participants were 243 patients who were not administered zinc supplement as part of the nutrition support team intervention between January 2010 and March 2019. The mean zinc level was 59.7μg/dl, and 66 subjects (27.2%) had pressure ulcers. Significant positive correlations were found between serum zinc level and albumin level, and between serum zinc level and pre-albumin level. The subjects were divided into the following groups according to their serum zinc level: Normal (≥ 80μg/dl), latent zinc deficiency (60 ≤ Zn < 80μg/dl), and zinc deficiency (< 60μg/dl). The zinc deficiency group had significantly lower serum albumin levels and pre-albumin levels. The zinc deficiency group had no difference in the amount of energy intake and protein intake. This suggests that the zinc absorption control mechanism failed for some reason, which makes it difficult for the body to maintain zinc homeostasis, and that this may be related to increased excretion of zinc. Our logistic regression analysis designed to search for factors that cause pressure ulcer led to the extraction of serum zinc level and albumin level as independent factors. There is a high possibility that zinc deficiency and malnutrition are related to the onset of pressure ulcer and increased severity, respectively. We believe that future studies on pressure ulcer treatment should focus on appropriate nutrition management and zinc supplementation.