PMID: 

J Nutr Metab. 2018 ;2018:9682975. Epub 2018 Oct 10. PMID: 30405910

Abstract Title: 

Zinc Deficiency and the Recurrence ofInfection after Fecal Microbiota Transplant: A Retrospective Cohort Study.

Abstract: 

Background: Fecal microbiota transplant (FMT) is an effective therapy for recurrentinfection (CDI). However, in 12% of patients treated with FMT, CDI recurs within one month. Zinc deficiency predicts increased diarrheal frequency in malnourished children, but little is known about its association with FMT outcome. We hypothesized that zinc levels were an independent predictor of CDI recurrence after FMT.Methods: We performed a retrospective cohort study of 80 patients (mean age, 66; 59 women) receiving FMT for CDI from 9/2013-9/2016 at a tertiary care center. Zinc levels were measured within 90 days before FMT. The primary outcome was CDI recurrence within 90 days after FMT. We controlled for risk factors for FMT failure using Cox regression. We also analyzed the effect of zinc supplementation in individuals with deficiency.Results: Forty-nine subjects had a normal zinc level, and 31 had a low level (

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PMID: 

Front Cell Neurosci. 2018 ;12:374. Epub 2018 Oct 22. PMID: 30405356

Abstract Title: 

Dietary Zinc Supplementation Prevents Autism Related Behaviors and Striatal Synaptic Dysfunction inExon 13-16 Mutant Mice.

Abstract: 

The SHANK family of synaptic proteins (SHANK1-3) are master regulators of the organizational structure of excitatory synapses in the brain. Mutations inare prevalent in patients with autism spectrum disorders (ASD), and loss of one copy ofcauses Phelan-McDermid Syndrome, a syndrome in which Autism occurs in>80% of cases. The synaptic stability of SHANK3 is highly regulated by zinc, driving the formation of postsynaptic protein complexes and increases in excitatory synaptic strength. As ASD-associated SHANK3 mutations retain responsiveness to zinc, here we investigated how increasing levels of dietary zinc could alter behavioral and synaptic deficits that occur with ASD. We performed behavioral testing together with cortico-striatal slice electrophysiology on amouse model of ASD (), which displays ASD-related behaviors and structural and functional deficits at striatal synapses. We observed that 6 weeks of dietary zinc supplementation inmice prevented ASD-related repetitive and anxiety behaviors and deficits in social novelty recognition. Dietary zinc supplementation also increased the recruitment of zinc sensitive SHANK2 to synapses, reduced synaptic transmission specifically through-methyl-D-aspartate (NMDA)-type glutamate receptors, reversed the slowed decay tau of NMDA receptor (NMDAR)-mediated currents and occluded long term potentiation (LTP) at cortico-striatal synapses. These data suggest that alterations in NMDAR function underlie the lack of NMDAR-dependent cortico-striatal LTP and contribute to the reversal of ASD-related behaviors such as compulsive grooming. Our data reveal that dietary zinc alters neurological function from synapses to behavior, and identifies dietary zinc as a potential therapeutic agent in ASD.

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PMID: 

Mol Med Rep. 2019 Jul ;20(1):655-663. Epub 2019 May 22. PMID: 31115566

Abstract Title: 

Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway.

Abstract: 

The high glucose (HG)‑induced epithelial‑mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) serves an important role in peritoneal fibrosis (PF) during peritoneal dialysis. Our previous study reported that zinc (Zn) supplementation prevented the HG‑induced EMT of rat PMCs in vitro. In the present study, the role of Zn in HG‑induced EMT was investigated in vivo using a rat model of PF. Additionally, the molecular mechanisms underlying HG‑induced EMT were studied in human PMCs (HPMCs). In the rat model of PF, HG treatment increased the glucose transfer capacity and decreased the ultrafiltration volume. Histopathological analysis revealed peritoneal thickening, increased expression of vimentin and decreased expression of E‑cadherin. ZnSO4 significantly ameliorated the aforementioned changes, whereas Zn inhibition by clioquinol significantly aggravated the effects of HG on rats.The effects of Zn on HPMCs was assessed using western blot analysis, Transwell assays and flow cytometry. It was revealed that Zn also significantly suppressed the extent of the EMT, and reduced reactive oxygen species production and the migratory ability of HG‑induced HPMCs, whereas Zn inhibition by N',N',N',N'‑tetrakis (2‑pyridylmethyl) ethylenediamine significantly potentiated the HG‑induced EMT of HPMCs. HG‑stimulated HPMCs exhibited increased expression of nuclear factor‑like 2 (Nrf2) in the nucleus, and total cellular NAD(P)H quinone dehydrogenase 1 (NQO1) and heme oxygenase-1 (HO‑1), the target proteins of the Nrf2 antioxidant pathway. Zn supplementation further promoted nuclear Nrf2 expression, and increased the expression of target proteins of the Nrf2 antioxidant pathway, whereas Zn depletion decreased nuclear Nrf2, NQO1 and HO‑1 expression compared withthe HG group. In conclusion, Zn supplementation was proposed to suppress the effects of HG on the EMT by stimulating the Nrf2 antioxidant pathway and subsequently reducing oxidative stress in PMCs.

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PMID: 

Am J Clin Nutr. 2019 Jun 4. Epub 2019 Jun 4. PMID: 31161192

Abstract Title: 

Zinc supplementation improves glycemic control for diabetes prevention and management: a systematic review and meta-analysis of randomized controlled trials.

Abstract: 

BACKGROUND: Although many studies have shown that low zinc status is associated with diabetes, the putative effects of zinc supplementation on glycemic control are inconclusive.OBJECTIVES: The aim of this meta-analysis of randomized controlled trials was to assess the effects of zinc supplementation in preventing and managing diabetes.METHODS: PubMed, Embase, and the Cochrane Library were searched for articles that were published through February 10, 2019 and contained estimates for the outcomes of interest. The pooled results were then analyzed with the use of a random-effects model.RESULTS: Thirty-two placebo-controlled interventions were extracted from 36 publications, involving a total of 1700 participants in 14 countries. Overall, compared with their respective control groups, the subjects in the zinc-supplementation group had a statistically significant reduction in fasting glucose [FG, weighted mean difference (WMD): -14.15 mg/dL; 95% CI: -17.36, -10.93 mg/dL], 2-h postprandial glucose (WMD: -36.85 mg/dL; 95% CI: -62.05, -11.65 mg/dL), fasting insulin (WMD: -1.82 mU/L; 95% CI: -3.10, -0.54 mU/L), homeostasis model assessment for insulin resistance (WMD: -0.73; 95% CI: -1.22, -0.24), glycated hemoglobin (WMD: -0.55%; 95% CI: -0.84, -0.27%), and high-sensitivity C-reactive protein (WMD: -1.31 mg/L; 95% CI: -2.05, -0.56 mg/L) concentrations. Moreover, subgroup analyses revealed that the effects of zinc supplementation on FG are significantly influenced by diabetic status and the formulation of the zinc supplement.CONCLUSIONS: Our analysis revealed that several key glycemic indicators are significantly reduced by zinc supplementation, particularly the FG in subjects with diabetes and in subjects who received an inorganic zinc supplement. Together, these findings support the notion that zinc supplementation may have clinical potential as an adjunct therapy for preventing or managing diabetes. This trial was registered at PROSPERO as CRD42018111838.

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PMID: 

Int J Prev Med. 2019 ;10:68. Epub 2019 May 17. PMID: 31198503

Abstract Title: 

Protective Effect of Zinc Supplementation on Renal Ischemia/Reperfusion Injury in Rat: Gender-related Difference.

Abstract: 

Background: Zinc (Zn) knows as essential microelement which prevents oxidative stress. The effect of Zn supplement on renal function parameters in rats subjected to renal ischemia-reperfusion (IR) injury was investigated.Methods: Male and female rats were subjected to renal IR with and without Zn sulfate (10 mg/kg/day for 5 days) supplementation. The kidney function markers and histology findings in Zn-treated group were compared with sham and control groups.Results: The serum levels of blood urea nitrogen and creatinine (Cr) and kidney tissue damage score were increased significantly after renal injury (

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Have you ever wished you could regenerate those brain cells you sacrificed in college? Do you fear that your aging brain is in a perpetual state of decline? Medical science is being rewritten to show that we CAN improve the health of our brain, and that repairing damage is not only possible, it’s something anyone can do.

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PMID: 

Pediatr Rep. 2019 May 23 ;11(2):7954. Epub 2019 May 23. PMID: 31214301

Abstract Title: 

A randomized controlled trial of zinc supplementation in the treatment of acute respiratory tract infection in Thai children.

Abstract: 

Acute Lower Respiratory Tract Infections (ALRI) are one of the most common causes of morbidity and mortality in young children. Zinc supplementation has been shown to have a preventive effect against respiratory infections, but little evidence is available on its effect on the treatment of ALRI. This study examined the effect of zinc supplementation on the treatment outcome in children that were hospitalized with ALRI. A randomized, doubleblinded, placebo-controlled trial was conducted on 64 hospitalized children with ALRI, who were aged between 2 and 60 months. Children were randomly allocated to receive zinc (30 mg elemental zinc/day) or placebo. The primary outcome was the time to the cessation of ALRI, while the secondary outcomes were the length of the stay in hospital and the individual features of the disease. The study found that ALRI cessation was faster in children who received zinc supplementation (median (IQR): 3 (2-4) days and 4 (3-5) days, respectively; P=0.008), and that their hospital stay was shorter (mean (SD): 3.8 (1.3) days and 6.1 (3.2) days, respectively; P

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PMID: 

Biol Trace Elem Res. 2019 Jul 30. Epub 2019 Jul 30. PMID: 31363990

Abstract Title: 

Zinc Supplementation Increased Bone Mineral Density, Improves Bone Histomorphology, and Prevents Bone Loss in Diabetic Rat.

Abstract: 

Diabetic osteoporosis (DOP) is a complication of diabetes, with the characteristics of bone mineral density (BMD) reduction and bone structure destruction. Zinc was reported has a benefit effect on postmenopausal osteoporosise, it was also has hypoglycemic effect, whether zinc was beneficial on diabetes-induced osteoporosis has not been reported. So in the present study, we established a diabetic rat model by streptozotocin injection (60 mg/kg), and administered zinc sulfate by oral gavage to investigate the protective effects of zinc on DOP and the underline possible mechanism. Thirty six Sprague Dawley rats were divided into T1DM group (diabetic rats), control group (vehicle treatment), and T1DM-Zinc group (diabetic rats administered zinc sulfate 0.25 mg/kg by oral gavage). The bone histomorphological parameters, serum bone metabolism markers (including ALP, OPG, RUNX 2, and RANKL), BMD, and bone marrow adipocyte numbers were detected after eight weeks of zinc sulfate treatment. The results showed zinc sulfate administration (0.25 mg/kg/d) decreased blood glucose, increased the BMD, decreased serum ALP, and RANKL, increased serum OPG and RUNX 2 levels, as well as OPG/RANKL ratio of T1DM rats. Meanwhile, the bone histomorphological parameters, bone marrow adipocytes numbers were returned to be normal. The RUNX 2, and OPG mRNA expression levels in bone tissues of T1DM-Zinc group rats were increased after zinc sulfate treatment compared with the diabetic rats (P 

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PMID: 

Int J Hematol. 2019 Aug 12. Epub 2019 Aug 12. PMID: 31407257

Abstract Title: 

Vitamin B6 deficiency is prevalent in primary and secondary myelofibrosis patients.

Abstract: 

Vitamin B6 (VB6) deficiency contributes to oncogenesis and tumor progression in certain cancers, and is prevalent in cancer patients in general. VB6 is also an essential element of heme synthesis, and deficiency can lead to anemia. Primary myelofibrosis (PMF) and secondary myelofibrosis (sMF) are myeloproliferative neoplasms often presenting with anemia along with other cytopenias. We performed a prospective study to determine whether PMF and sMF patients suffer from VB6 deficiency, and whether VB6-deficient patients show improvement of anemias with VB6 supplementation. Twelve PMF patients and 11 sMF patients were analyzed. A total of 16 of 23 patients (69.6%) were found to have VB6 deficiency, but VB6 supplementation with pyridoxal phosphate hydrate did not elevate hemoglobin levels in deficient patients. None of the patients presented with vitamin B12, iron, or copper deficiencies. Four patients showed serum folate levels below the lower limit of normal and eight patients showed serum zinc levels below the lower limit of normal; however, these deficiencies were marginal and unlikely to contribute to anemia. Compared to VB6-sufficient patients, VB6-deficient patients showed significantly lower serum folate levels and higher serum copper levels. Studies elucidating the relationship of VB6 deficiency and etiology of PMF/sMF are warranted.

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PMID: 

Acta Neurol Belg. 2019 Jul 13. Epub 2019 Jul 13. PMID: 31302864

Abstract Title: 

The role of zinc supplementation on the metallothionein system in children with autism spectrum disorder.

Abstract: 

The present research was carried out to elucidate the role of zinc (Zn) supplementation on the plasma concentration and gene expression, as well as the effects on cognitive-motor performance, in a cohort of children with autism spectrum disorder (ASD). The study was performed on a cohort of 30 pediatric subjects with ASD, encompassing an age range of 3-8 years. The impact of Zn supplementation was investigated in 3 months (or 12 weeks) on the ASD children. Each daily dosage of Zn was calculated as being equal to the body weight in kg plus 15-20 mg. The effect of Zn was also evaluated on the serum level of metallothionein 1 (MT-1A), and the severity of autism via scores on the Childhood Autism Rating Scale. The effect of Zn was investigated on the gene expression of MT1-A before and after Zn supplementation. The data of the present study showed an increase in cognitive-motor performance and an increased serum metallothionein concentration,as well as a significant lowering in the circulating serum levels of copper (Cu) following Zn supplementation. In the cohort of ASD patients, the genetic expression of MT-1 was higher after Zn therapy than before the treatment. In conclusion, Zn supplementation might be an important factor in the treatment of children with ASD.

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