Metabolomics Workbench ST000330 - GNPS - Effects of Zinc on GI tract metabolites (Part 1: Esophagus)
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q-TOF - NEGATIVE, Q-TOF - POSITIVE
ORGANISM(S): Mus Musculus
SUBMITTER: 
Oliver Fiehn
PROVIDER: MSV000082696 | GNPS | Thu Aug 02 17:07:00 BST 2018
REPOSITORIES: GNPS
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Project description:This experiment tested the affects of different diets on mice esophagus metabolites. The diets ranged from zinc sufficient to zinc deficient and a third group that included zinc deficient mice that were put back on zinc sufficient diets.
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Project description:Nutritional status influences feeding behaviors, food preferences and taste sensations. For example, zinc-deficient rats have been reported to show reduced and cyclic food intake patterns with increased preferences for NaCl. Although some impairments of the central nervous and endocrine systems have been speculated to be involved in these phenomena, the effects of short-term zinc deficiency on the brain have not been well examined to date. In this study, we performed a comprehensive analysis of the gene expression patterns in the rat diencephalon, which is a portion of the brain that includes the hypothalamus and thalamus, after short-term zinc deficiency and also during zinc recovery. The rats showed reduced and cyclic food intake patterns with increased salt preferences after a 10-day dietary zinc deficiency. A comparative analysis of their diencephalons using cDNA microarrays revealed that approximately 1% of the genes expressed in the diencephalons showed significantly altered expression levels. On the other hand, a 6-day zinc supplementation following the deprivation allowed for the recovery to initial food intake behaviors and salt preferences. The expression levels of most of the genes that had been altered by exposure to zinc deficient conditions were also recovered. These results show that feeding behaviors, taste preferences and gene expression patterns in the diencephalon respond quickly to changing zinc levels. This suggests that the gene expression changes observed in the diencephalon and the accompanying functional changes may be related to the development of deviations in feeding behaviors and increased preferences for NaCl in zinc-deficient rats. Four-week-old male Sprague-Dawley rats were purchased from Charles River Japan (Yokohama, Japan). Fifteen rats were individually housed in a stainless steel cage in a room with constant humidity at 22 ± 1 °C under a 12 h light-dark cycle (lights on at 8:00). Zinc-deficient diets (# D19488M, Research Diets, New Brunswick, NJ, USA) were based on the AIN-93G diet and contained 0.6 mg zinc / 1000 g diet (Table 1). For the control zinc-sufficient diets, zinc sulfate supplements were provided with up to 30.0 mg zinc / 1000 g diet. Rats were fed the control diets ad libitum for 1 week for adaptation and then were divided into two groups matched for body weight. For the zinc-deficient experiment, rats in the ZD group (n =9) were allowed to eat the zinc-deficient diets ad libitum. The rats in the PF group (n = 6) were pair-fed the control diets to match the intake of the ZD rats. Two fluid bottles with deionized water were attached to each cage for the entire experiment with the exception of the 48 h preference test, in which 300 mM NaCl was provided from days 6 to 8. Zinc was limited for 10 days to reduce the effects of differences in salt intake in the preference test between the two groups. For the zinc recovery experiment, the ZR (n = 9) and ZRPF (n = 6) groups were subjected to the same conditions as above. Briefly, after 1 week of adaptation, ZR rats were fed the zinc-deficient diets ad libitum, and ZRPF rats were pair-fed the control diets for 10 days. After that, the rats in both the ZR and ZRPF groups were fed the fixed amount (13 g) of the control diets for the 6 day zinc recovery period to avoid any differences in food intake between the two groups that would be caused by pair-feeding because the previous report showed rapidly increased food intake following the initiation of the zinc-sufficient diets after zinc deficiency [1]. The diet amounts were restricted to the average consumption of the ZR group on the last day of the zinc-deficient period. The 48 h two-bottle preference tests for 300 mM NaCl were performed from days 6 to 8 during the deficient period and from days 14 to 16 during the recovery period. The analysis removed one rat from the ZRPF group showing more than a 0.5 of preference ratio to the 300 mM NaCl solution and three rats from the ZR group showing less than 0.5 preference ratios as assessed by a preference test that was conducted during days 6 to 8. At the end of each experiment, the rats were deeply anesthetized with pentobarbital sodium. Blood samples were collected from the carotid arteries and stored at -80 °C. The brains were quickly removed from the bodies after decapitation, and the diencephalons were separated by forceps on ice. The diencephalons were washed in ice-cold phosphate-buffered saline (PBS), treated with RNAlater (Invitrogen, Carlsbad, CA, USA), and stored at -20 °C. The serum zinc concentrations were analyzed with an ICP-AES (SPS 1200 VR, Seiko Instruments, Chiba, Japan). The Animal Care Committee of the University of Tokyo approved all animal experiments. Four average rats from each group were selected based on body weights, plasma zinc concentrations, and salt preferences.
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Project description:A common reference model was used to design the microarray experiment, in which cDNA from T. caerulescens roots exposed to 100 uM (sufficient) zinc was used as the common reference. Every slide was always hybridized with the common reference sample and with a sample from one of the treatments (Arabidopsis or T. caerulescens exposed to deficient, sufficient or excess zinc). The common reference was labeled with the fluorescent dye Cyanine 3 (Cy3) and the treatment samples were labeled with Cyanine 5 (Cy5). As a quality control step we performed a dye-swap hybridization for one sample (from T. caerulescens roots exposed to sufficient zinc).
2006-10-10 | E-MEXP-877 | biostudies-arrayexpress
Project description:Weanling littermates Cox-2-/- and Cox-2+/+ (WT) mice were fed a zinc-deficient (ZD) or zinc-sufficient (ZS) diet to form 4 groups, namely, ZD:Cox-2-/- (n=4), ZD:WT (n=4), ZS:Cox-2-/- (n=4) and ZS:WT (n=4). After 8 weeks, ZD mouse forestomach evidenced increased cell proliferation as demonstrated by increased proliferating cell nuclear antigen [PCNA] labeling. The mice were sacrificed and forestomachs isolated. Forestomach epithelia were prepared by using a blade to strip off the submucosal and muscularis layers under the guidance of a dissecting microscope. We performed microarray analysis on individual RNA samples prepared from 4 mice from each of the following 4 groups: ZS:Cox-2-/-, ZS:WT, ZD:Cox-2-/- and ZD:WT mice (n=4/group), using GeneChipï¾® Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA). All RNA samples displayed intact ribosomal RNA 18S and 28S bands as determined by the Agilent 2100 Bioanalyzer. Five micrograms of total RNA was reverse transcribed into cDNA followed by in vitro transcription and labeling to produce biotin-labeled cRNA using IVT Labeling Kit. The labeled cRNA was hybridized to the array, followed staining with streptavidin-phycoerythrin. The distribution of fluorescent material on the oligonucleotide probes sets was obtained using GeneArray Scanner
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Project description:LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age-matched wildtype mice on a vitamin A sufficient diet
2016-07-25 | GSE74905 | GEO
Project description:LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age and gender matched wildtype mice on a vitamin A sufficient diet
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Project description:Mouse Iron Distribution Dynamics
Dynamic model of iron distribution in mice. This model attempts to fit the radioiron tracer data from Lopes et al. 2010 for mice fed iron deficient and rich diets by adjusting the rate of iron intake (vDiet) and the hepcidin synthesis rate (vhepcidin) independently for each experiment. All other parameters are those that provide the best fit for the adequate diet.
This model includes the radioiron tracer species.
Differences in parameter values between deficient, rich, and adequate diets:
Diet
vDiet
vhepcidin
Adequate
0.00377422
1.7393e-08
Deficient
0
8.54927e-09
Rich
0.00415624
2.30942e-08
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Project description:Zinc deficiency during pregnancy and postnatal life can adversely affect the health and predispose to an increased risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes with the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague-Dawley (SD) rats. Pregnant females SD were allocated into three groups: dams received diets containing adequate (35 mg/Kg chow), deficient (3 mg/Kg chow) or supplemented (180 mg/Kg chow) zinc levels during gestational day 10 (GD 10) until the litters weaning. Female offspring were allocated into three groups and received the same diets as their dams until postnatal day (PND) 51. At PND 51, females SD (n=16 each group) received a single dose of DMBA (50 mg/kg, ig) for initiation of mammary carcinogenesis, adequate zinc diets and were euthanized at PND 180. Tumors samples were collected and processed for histological evaluation and microarray analysis. Dietary zinc deficiency induced a significant reduction in female offspring body weight evolution at parturition, weaning and pubertal phases. At late in life, the early in life dietary zinc deficiency or supplementation did not alter the latency, incidence, multiplicity and volume or histological types of mammary tumors in relation to the adequate zinc group, and changed the expression of a small amount of genes. The present findings indicate that early-in life dietary zinc deficiency or supplementation did not significantly modify the susceptibility to development of mammary tumors induced by DMBA.
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