Effects of zinc deficiency on gut microbiota of school-age children
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB51060 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR8766560_1.fastq.gz | Fastqsanger.gz | |||
| ERR8766560_2.fastq.gz | Fastqsanger.gz | |||
| ERR8766570_1.fastq.gz | Fastqsanger.gz | |||
| ERR8766570_2.fastq.gz | Fastqsanger.gz | |||
| ERR8766580_1.fastq.gz | Fastqsanger.gz |
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Project description:Injury occurring during critical periods of development may have long-term effects on inflammatory responses. Periventricular leukomalacia (PVL) is the most common cause of cerebral palsy (CP) in preterm infant. Activated leukocytes are the main source of inflammatory cytokines that give rise to white matter damage and CP in preterm infant. Here, we tested the hypothesis that inflammation profiles as pathogenic mediators for the occurrence of PVL in the neonatal period may persist in preterm children with CP at school age. Five preterm children with PVL-induced CP and gestational age-matched five preterm children with normal neurodevelopment were recruited from follow up clinics. Proinflammatory gene expression in the PBMCs from preterm children were determined by Superarray PCR study.
2010-05-22 | E-GEOD-17390 | biostudies-arrayexpress
Project description:Injury occurring during critical periods of development may have long-term effects on inflammatory responses. Periventricular leukomalacia (PVL) is the most common cause of cerebral palsy (CP) in preterm infant. Activated leukocytes are the main source of inflammatory cytokines that give rise to white matter damage and CP in preterm infant. Here, we tested the hypothesis that inflammation profiles as pathogenic mediators for the occurrence of PVL in the neonatal period may persist in preterm children with CP at school age.
2009-09-30 | GSE17390 | GEO
Project description:The supragingival plaque microbiota of pre-school children.
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Project description:We tested a hypothesis that prenatal alcohol exposure may lead to epigenetic alterations to the DNA resulting in attentional and cognitive alterations of the children. 6-9 year old children school children of the Franconian Cognition and Emotion Studies (FRANCES) cohort which were tested for an objective marker of PAE, ethyl glucuronide (EtG) in meconium at birth. 32 newborns were found to be exposed to alcohol with a threshold above 30 ng/g (EtG+) but without a FAS diagnosis. DNA for methylation analysis was extracted from buccal cells, DNA methylation was analyzed using the Infinium Human Methylation 450K BeadChip array (Illumina).
2018-05-12 | E-MTAB-6730 | biostudies-arrayexpress
Project description:Preventive zinc supplementation provided as a stand-alone dispersible tablet, or via home fortification as multiple micronutrient powders (MNPs), has been considered a potential strategy to prevent zinc deficiency and improve health (including immune) outcomes among children in low- and middle-income countries. However, the impact of zinc supplementation on immune profiles has not been well characterised. We sought to define the effect of zinc supplementation on peripheral blood gene expression among young children in Dhaka, Bangladesh. In a sub study of a large randomized, controlled, community-based efficacy trial where children 9-11 months of age received one of the following interventions on a daily basis for 24 weeks 1) MNPs containing 10 mg of zinc; 2) dispersible tablet containing 10 mg zinc; or 3) placebo powder, we used RNA-sequencing to profile the peripheral blood gene expression, as well as highly sensitive multiplex assays to detect cytokine profiles. We profiled samples from 100 children enrolled in the parent trial. We did not detect an effect from either zinc intervention on differential peripheral blood gene expression at the end of intervention, or an effect from intervention on change in gene expression from baseline. We also did not detect an effect from either intervention on cytokine concentrations. Exploratory analysis did not identify an association between undernutrition (defined as stunting, underweight or wasting) on peripheral blood gene expression.
2021-10-27 | GSE184998 | GEO
Project description:Zinc is an essential trace micronutrient and exerts important physiological and biochemical roles. Zinc deficiency is a global public-health problem. Standing untreated zinc deficiency can cause series adverse effects, including growth retardation, poor appetite, delayed sexual development, impaired neurologic and immune systems, diabetes and obesity, et al. However, the underlying mechanisms of these adverse effects remain elusive in most cases and a comprehensive understanding of the adverse effects (known and unknown) induced by zinc deficiency is lacking. As we know, zinc is a critical component of over 3000 enzymes and is required for numerous catalytic, structural, and regulatory functions of proteins. Thus, the impairments in enzyme actions are responsible for the gross symptoms of zinc deficiency. Altered enzymes may induce to the extensive changes in diverse molecular components of body, including DNA, mRNA and metabolites; and all above changes may work together to induce the adverse effects and affect the health of body. Therefore, protein changes associated with zinc deficiency are very necessary to be unraveled and described for revealing the known and unknown adverse effects and underlying mechanisms. In this project, we first performed a multi-omics study by integrating plasma metabolomics and proteomics, liver proteomics and metal ionomics on zinc deficient rats in order to identify biomarkers (proteins, metabolites and metal elements) of zinc deficiency and reveal the changed metabolic pathways. Eventually, we expected to completely present known adverse effects and their underlying molecular mechanisms, and uncover unknown adverse effects of zinc deficiency.
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Project description:Gut microbial diversity among school children of Tibetan, Hui, and Han ethnics in the Qinghai˗Tibetan Plateau
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Project description:Zinc is an essential trace element that is closely related to learning and memory ability. The hippocampus plays an important role in learning and memory and has the highest zinc concentration in the brain. Severe zinc deficiency (zinc-deprived diet) significantly alter hippocampal protein expression and impair learning and memory abilities. However, no study has investigated the effects of marginal zinc deficiency (low zinc diet) on hippocampal proteins and learning and memory abilities. In this study, the rat model after 4 and 8 weeks of feeding with low zinc diet was first used to identify and quantify the hippocampal proteins of low zinc rats by high-thoughput proteomics technology. Explore the changes of hippocampus proteome patterns after 4 and 8 weeks of feeding with low zinc diet were compared with those in control rats.
2021-10-04 | PXD028998 |
Project description:Zinc deficiency could lead to a dynamic variation in gut microbial composition and function in animals. However, how zinc deficiency affects the gut microbiome in school-age children remains unclear. The purpose of this study was to profile the dynamic shifts in the gut microbiome of school-age children with zinc deficiency, and to determine whether such shifts are associated with dietary intake. A dietary survey, anthropometric measurements, and serum tests were performed on 177 school-age children, and 67 children were selected to explore the gut microbial community using amplicon sequencing. School-age children suffered from poor dietary diversity and insufficient food and nutrient intake, and 32% of them were zinc deficient. The inflammatory cytokines significantly increased in the zinc deficiency (ZD) group compared to that in the control (CK) group (p < 0.05). There was no difference in beta diversity, while the Shannon index was much higher in the ZD group (p < 0.05). At the genus level, Coprobacter, Acetivibrio, Paraprevotella, and Clostridium_XI were more abundant in the ZD group (p < 0.05). A functional predictive analysis showed that the metabolism of xenobiotics by cytochrome P450 was significantly depleted in the ZD group (p < 0.05). In conclusion, gut microbial diversity was affected by zinc deficiency with some specific bacteria highlighted in the ZD group, which may be used as biomarkers for further clinical diagnosis of zinc deficiency.
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Project description:Zinc is an essential nutrient because of its role in catalysis and in stabilizing protein structure, but excess zinc can also be deleterious. Four nutritional zinc states have been identified in the alga Chlamydomonas reinhardtii: zinc toxic, zinc replete, zinc deficient and zinc limited. Growth is inhibited in zinc-limited and zinc toxic cells relative to zinc-replete cells, while zinc-deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition responsive changes in gene expression. We identified a subset of genes encoding zinc-handling components, including ZIP family transporters and candidate zinc chaperones. In addition, we noted an impact on two other regulatory pathways, the carbon concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc-deficiency, as a likely consequence of reduced carbonic anhydrase activity, which is validated by mass spectrometry and immunoblot analysis of Cah1, Cah3 and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in air in zinc limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. Surprisingly, we noted also that the Crr1 regulon, which responds to Cu limitation, is also turned on in zinc deficiency, and in fact, Crr1 is required for growth in zinc-limiting conditions. Zinc deficient cells are functionally copper deficient, as evidenced by reduced plastocyanin abundance, even though they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester Cu in a bio-unavailable form, perhaps to prevent mis-metallation of critical zinc sites. Zn-limited wild-type cells were generated by transfer of cells from the first round of growth in medium with no supplemental Zn into TAP medium supplemented or not with 2.5 µM Zn-EDTA The control samples for this study are represented in GSE25622
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