Vitamin A-deficient diet
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE1600 | GEO | 2005/06/30
SECONDARY ACCESSION(S): PRJNA90335
REPOSITORIES: GEO
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Project description:Analysis of livers from 74-day old male rats fed vitamin A sufficient or vitamin A deficient diet for 53 days. Either 10ug or 2ug of total RNA used in standard Affymetrix protocol
2007-11-01 | E-GEOD-1600 | biostudies-arrayexpress
Project description:The aim of the study was to investigate the role of vitamin D on adipocyte development. To this end, rat dams (Sprague-Dawley rats ) were fed diets with 0 or 1,000 IU vitamin D3 per kg diet 5 weeks prior to conception until the end of lactation. By using high-density DNA microarrays, we analyzed the gene-expression profile of mesenterial adipose tissue of both groups of newborn rats.
2016-12-31 | GSE82215 | GEO
Project description:Astaxanthin alleviates hepatic lipid accumulation and peroxidation, inflammation, and fibrosis in mice with high-cholesterol, high-cholate, and high-fat (CL) diet-induced nonalcoholic steatohepatitis (NASH). It has been proposed as a potential new treatment to inhibit the progression of NASH in humans. Therefore, we compared hepatic gene expression profiles after treatment with astaxanthin or the antioxidant vitamin E in mice with CL diet-induced NASH. Comprehensive gene expression analyses of the livers of mice fed a standard, CL, or CL diet containing astaxanthin or vitamin E for 12 weeks were performed using a DNA microarray. Both astaxanthin and vitamin E effectively improved gene expression associated with eukaryotic initiation factor-2 (EIF2) signaling, which is suppressed in NASH by endoplasmic reticulum (ER) stress in the liver. Astaxanthin but not vitamin E was predicted to suppress the actions of ligand-dependent nuclear receptors peroxisome proliferator-activated receptors (PPAR) α and PPARδ and to affect related molecules. Establishing a new therapy using astaxanthin will require elucidation of astaxanthin’s molecular action on the functions of PPARα and related molecules in the livers of mice with diet-induced NASH.
2017-03-21 | GSE93819 | GEO
Project description:Background: In addition to its canonical functions, vitamin D has been proposed to be an important mediator of the immune system. Despite ample sunshine, vitamin D deficiency is prevalent (> 80%) in the Middle East, resulting in a high rate of supplementation. However, the underlying molecular mechanisms of the specific regimen and potential factors affecting an individual’s response to vitamin D are not well characterized. Objective: To characterize changes in blood transcriptomic and the potential mechanisms associated with vitamin D3 supplementation and response. Design: In this intervention study, one hundred vitamin D-deficient women were given a weekly oral dose (50,000 IU) of vitamin D3 for three months. A high-throughput targeted PCR, composed of 264 genes representing important blood transcriptomic fingerprints in health and disease states, was performed on pre- and post-supplementation blood samples to profile the molecular response to vitamin D3. Multivariate, network, gene ontology, and literature mining analyses were used for the interpretation of the transcriptomic profiling results. Results: We identified 54 differentially expressed genes that were strongly modulated by vitamin D3 supplementation. Network analyses showed significant changes in the immune-related pathways such as TLR4/CD14 and IFN receptors, and catabolic processes related to NFkB, which were subsequently confirmed by gene ontology enrichment analyses. We proposed a model for vitamin D3 response, using the reduced expression of the molecules involved and the receptor-mediated intra-cellular signaling leading to reduce cytokine production. Conclusions: Blood-transcriptomic profiles of vitamin D3 response were generated using a targeted blood gene panel. Vitamin D has a strong effect on the immune system, G-coupled protein receptor signaling, and the ubiquitin system. We highlighted the major molecular changes and biological processes induced by vitamin D3, which will help to further investigate the effectiveness of vitamin D supplementation among individuals in the Middle East.
2021-05-19 | GSE157939 | GEO
Project description:Vitamin A deficiency is detrimental to the visual system throughout the lifecycle. Abundant expression of the retinoid transporter STRA6 in the retinal pigment epithelium (RPE) and homeostatic blood levels of retinol binding protein ensure the eyes are adequately supplied with the nutrient. STRA6 deficiency interrupts the supply pathway, but vitamin A in chylomicrons compensates for its failure. However, dependency on the chylomicron delivery pathway makes the eyes of STRA6-deficient mice vulnerable to dietary vitamin A deprivation. How the eyes adapt to vitamin A status has not been studied in molecular detail, and therefore we used RNA-seq to focus on diet-induced changes. We observed that mild ocular vitamin A deficiency was linked to an increase in transcript abundance levels of genes coding for proteins of stress pathways and a decrease in levels of transcripts coding for proteins of pathways of visual sensitivity and perception. These changes correlate with a loss of visual sensitivity and accumulation of fluorescent debris in the retina. Additionally, severe vitamin A deficiency decreased the transcript levels of genes involved in cell adhesion, cell differentiation, and transport of small molecules pathways. This response correlated with alterations in epithelial cell morphology and a “leaky” RPE barrier. Together, our analyses of STRA6-deficient mice define adaptive responses associated with ocular vitamin A status and reveal a previously unknown role of STRA6 in the maintenance and functioning of the outer blood-retina barrier.
2023-06-07 | GSE219252 | GEO
Project description:The open chromatin of mouse longterm hematopoietic stem cells in control and vitamin A deficiency has been profiled by ATAC-seq.
2021-11-02 | E-MTAB-9780 | biostudies-arrayexpress
Project description:Initiation of a vitamin A deficient diet in mid-gestation, maintained in the post-weaning diet is sufficient to cause liver and serum retinoid depletion. Wild type C57Bl/6J timed mated pregnant dams were administered either a defined vitamin A sufficient low fat (12 percent kcal from fat) diet or matched vitamin A deficient diet from embryonic day 10.5. Vitamin A sufficient offspring were weaned onto either a high fat diet (60 percent kcal from fat) or maintained on the low fat 12 percent kcal from fat diet for 11 weeks (14 weeks of age). Gestational vitamin A deficient offspring were maintained on the same vitamin A deficient diet until 14 weeks of age. The impact of the maternal diet on a post-weaning high fat diet was compared to a standard maternal breeder diet followed by the post-weaning high fat diet.
2016-10-12 | GSE87845 | GEO
Project description:Clontech Atlas Stress array of rat distal colon of rats fed on vitamin E sufficient or deficient diets. Keywords: ordered
2004-12-31 | GSE1063 | GEO
Project description:Analysis of gene expression in skin of rats subjected to electron irradiation and the effect of vitamin A supplements. Keywords: other
2003-03-20 | GSE284 | GEO
Project description:Vitamin D, a fat-soluble vitamin, plays a critical role in calcium homeostasis, the immune system, and normal development. Many epidemiological cohort studies globally have found high prevalence rates of vitamin D deficiency and insufficiency, recognized as an important health issue that needs to be solved. In particular, reproductive age and pregnant women low in vitamin D status may confer risks of diseases like obesity on their offspring. While observational studies have suggested associations between prenatal vitamin D deficiency and metabolic phenotypes in offspring, not yet determined is whether prenatal vitamin D deficiency permanently alters the development of the liver, a major metabolic organ. We tested the histopathology and the transcriptomic profiles of livers from male C57BL/6J mice exposed to prenatal vitamin D deficiency through a maternal dietary intervention model. We found that prenatal vitamin D deficiency increases the prevalence of histopathological changes in the liver, and alters its gene expression profile. Cell subtype proportion analysis showed that the liver of prenatal vitamin D deficiency alters non-parenchymal cells of the liver, specifically macrophages, a subset of endothelial cells, and dendritic cells. Our results indicate the long-term memory of prenatal vitamin D deficiency exposure in the adult liver, a potential contributor to offspring health risks.
2022-05-10 | GSE194417 | GEO