Rattus norvegicus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-31430
PROVIDER: PRJNA145789 | ENA |
REPOSITORIES: ENA
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Project description:Dietary zinc status reversibly alters both the feeding behaviors of the rats and gene expression patterns in diencephalon
2015-09-18 | E-GEOD-31430 | ExpressionAtlas
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.
2011-12-01 | GSE31430 | GEO
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.
2011-12-01 | E-GEOD-31430 | biostudies-arrayexpress
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 | iProX
Project description:This study analyzed gene expression of rat peripheral blood mononuclear cells by microarray analysis following different feeding conditions (ad libitum feeding, fasting and refeeding) in normoweight (control) and in diet-induced obese rats (cafeteria rats). The aim of this study was to identify genes and biological pathways that were altered by feeding conditions in normoweight and diet-induced obese rats. Keywords: Dietary treatment, analysis of feeding conditions
2009-12-31 | GSE14497 | GEO
Project description:Maternal exposures during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. We investigated whether feeding pregnant rats a high fat (HF) or ethinyl-estradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. Here we show that mammary tumorigenesis is higher in daughters and granddaughters of HF rat dams and in daughters, granddaughters and great-granddaughters of EE2 rat dams. Outcross experiments indicate that increased mammary cancer risk is transmitted to HF granddaughters equally through the female or male germlines, but it is only transmitted to EE2 granddaughters through the female germline. The effects of maternal EE2 exposure on offspring's mammary cancer risk are associated with alternations in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and estrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through non-genetic means We examined the whole genome methylation status of both control and EE2-supplemented diet rats in three consecutive generations
2012-09-20 | E-GEOD-40251 | biostudies-arrayexpress
Project description:Even though the importance of adequate zinc intake has been known for around half a century, a reliable diagnostic tool to assess the dietary zinc status of individual humans or populations is in absence. The specific aim of this study was to examine differential expression of specific gene transcripts that occur when the dietary intake of zinc is acutely reduced below the dietary requirement for a period of ten days. Gene expression profiles of whole blood collected before and after dietary zinc restriction were determined by microarray analyses. The data provide potential signature genes of suboptimal zinc consumption and relevant bioinformatic interpretation indicate immune response and cell cycle regulation as biological processes associated with the zinc-responsive genes. To identify candidate markers holding the potential to indicate zinc status, a 24-day observational study comprised of acclimation (7 d; 10.4 mg Zn/d), zinc depletion (10 d; 0.3 mg Zn/d), and zinc repletion (7 d; 29.5 mg Zn/d) phases was conducted with healthy male subjects (n = 9). On day 0, 6 and 10 of zinc depletion, whole blood was collectedunder morning fasting state. RNA profiles were stabilized by using PAXgene reagents during the collection process and globin RNA reduction was conducted to improve the detection of transcripts at low abundance. Genes responding to dietary zinc restriction were determined by array results from individual samples collected before and after 10 d of zinc depletion. Pooled RNA samples from each day of blood collection, i.e., baseline, 6 d and 10 d of depletion, respectively, were used to determine the temporal expression pattern of the zinc-responsive genes during dietary zinc depletion.
2011-11-15 | E-GEOD-33174 | biostudies-arrayexpress
Project description:Even though the importance of adequate zinc intake has been known for around half a century, a reliable diagnostic tool to assess the dietary zinc status of individual humans or populations is in absence. The specific aim of this study was to examine differential expression of specific gene transcripts that occur when the dietary intake of zinc is acutely reduced below the dietary requirement for a period of ten days. Gene expression profiles of whole blood collected before and after dietary zinc restriction were determined by microarray analyses. The data provide potential signature genes of suboptimal zinc consumption and relevant bioinformatic interpretation indicate immune response and cell cycle regulation as biological processes associated with the zinc-responsive genes.
2011-11-15 | GSE33174 | GEO
Project description:Background: 2,5-Dimethyl-4-hydroxy-3(2H)-furanone (DMHF) is one of the major odor compounds generated by the Maillard reaction. We previously reported that the inhalation of DMHF decreased systolic blood pressure via the autonomic nervous system in rats. The autonomic nervous system is also closely related to appetite regulation. The present study investigated the effects of DMHF on dietary intake and gene expression. Results: The inhalation of DMHF increased the dietary intake of rats during the feeding period. However, body weight gain was suppressed after six weeks of feeding. A DNA microarray analysis showed that DMHF altered gene expression associated with feeding behavior and neurotransmission in the rat brain. Conclusion: DMHF inhalation promotes appetite and changes gene expression in rats. Furthermore, phenotypic changes may regulate neurotransmission and appetite at the mRNA level in addition to controlling the autonomic nervous system.
2020-04-01 | GSE138482 | GEO
Project description:Diets rich in carbohydrates not only lead to obesity but also contribute to the liver metabolic diseases. Starch is the major energy source of the daily diet. However, little is known about the metabolic changes due to the intake of different dietary starches. Our aim was to assess the overall metabolic changes at the transcriptome level. Animal model was used, and a total of 16 weaned pigs were randomly allotted to two experimental diets containing either of cassava starch (CS) or maize starch (MS) during 21 days. At the end of the trial, liver tissues were sampled and used for analysis of digestive enzymes, metabolites and transcriptomes. The growth performance was not affected by dietary starch sources. However, CS-feeding significantly increased the serum insulin and cholesterol concentrations (P<0.05). The liver triglyceride and cholesterol content were both elevated by CS-feeding (P<0.05). Microarray analysis led to the identification of 648 genes differentially expressed in liver (P<0.05). The CS-feeding activated the transcription of lipogenic genes such as HMGR and FASN, but decreased the expression of lipolytic genes such as ACOX1, PPARA and FBP. The microarray results correlated well with the measurements of several key enzymes involved in hepatic lipid metabolisms. These results suggested that dietary starch source alters hepatic transcriptome in weaned pigs. The slowly digestible starch (i.e. MS) seemed to be more healthful for mammals as the dietary energy supplier by transcriptional down-regulation of lipogenesis and steroidogenesis.
2010-03-11 | GSE20721 | GEO