EGSB reactor biomass subjected to caffeine, aspartame, sucralose and cyclamate.
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PROVIDER: PRJNA1294778 | ENA |
REPOSITORIES: ENA
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Project description:Sucralose is an artificial sweetener commonly used in food and drinks to increase food palatability and control total calorie content. While it is approved for human consumption by both the EFSA and the FDA, recent reports have questioned the safety of long-term consumption of s. in this study, we show that high doses of sucralose affect immune responses in different mouse models of autoimmunity, infection, and cancer. Similarly, sucralose impedes proper t cell proliferation and polarization in vitro. Mechanistically, sucralose dampens signals downstream the TCR resulting in decrease calcium flux upon TCR activation.
2023-03-14 | GSE220862 | GEO
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Project description:Aspartame is a non carbohydrate artificial sweetener widely used in medicine and food. Some scholars believe that aspartame has neurotoxicity, mainly due to the presence of phenylalanine in its metabolites, which can pass through the blood-brain barrier, change the brain amino acid ratio, and interfere with neurotransmitter transmission. However, whether aspartame has an impact on human innate immunity is still unknown. This experiment will use Caenorhabditis elegans as a model to study its effect on innate immunity and provide reliable data support for the safety of aspartame as a sweetener.
2025-12-31 | GSE273859 | GEO
Project description:Aspartame has been widely used as a sweetener in foods and beverages since the 1980s. In this study, we aimed to assess the effect of aspartame on gut epithelial cell biology, inflammation, and the epithelial barrier. Aspartame shows cytotoxic effects and epithelial barrier damage as well as proinflammatory cytokine release in gastrointestinal epithelial cells, organoids and organ-on-a-chips at concentrations corresponding to daily used doses in food products. Cellular cytotoxicity was observed in as low as 1.25 mg/ml doses. RNA sequencing analysis revealed that aspartame significantly altered the transcriptome in gut-on-a-chip models, showing upregulation of pathways such as unfolded protein response, activated pro-apoptotic and inflammatory, and downregulation of DNA repair and replication mechanisms pathways. Aspartame exposure upregulated proinflammatory genes, particularly in the TNF signalling pathway, and induced multiple chemokine responses. It activated the NF-κB pathway via oxidative stress, promoting inflammation on NF-κB reporter monocyte cells and causing gut epithelial cell death. Aspartame affected genes involved in tight and adherens junctions, disrupting gut epithelial barrier integrity in a dose-dependent manner in gut-on-a-chip models. Additionally, aspartame suppressed key DNA repair and replication genes involved in double-strand break repair, mismatch repair, and DNA replication. Overall, our findings indicate that at commonly consumed levels, aspartame induces cellular stress, inflammation, and epithelial barrier damage in gastrointestinal epithelial cells. These findings underscore the biological relevance of our results and raise concerns that daily dietary intake of aspartame may pose previously underappreciated risks to gut health.
2026-01-01 | GSE285905 | GEO
Project description:Non-nutritive sweeteners like sucralose are consumed by billions of people. While animal and human studies have demonstrated a link between synthetic sweetener consumption and metabolic dysregulation, the mechanisms responsible remain unknown. Here we use a diet supplemented with sucralose to investigate the long-term effects of sweet/energy imbalance. In flies, chronic sweet/energy imbalance promoted hyperactivity, insomnia, glucose intolerance, enhanced sweet taste perception and a sustained increase in food and calories consumed, effects that are reversed upon sucralose removal. Mechanistically, this response was mapped to the ancient insulin, catecholamine, and NPF/NPY systems and the energy sensor AMPK, which together comprise a novel neuronal starvation response pathway. Interestingly, chronic sweet/energy imbalance promoted increased food intake in mammals as well, and this also occurs through an NPY-dependent mechanism. Together our data show that chronic consumption of a sweet/energy imbalanced diet triggers a conserved neuronal fasting response and increases the motivation to eat.
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Project description:We show that daily exposure of mice to aspartame, an artificial sweetener found in over 5,000 diet foods and drinks at doses equivalent to only 15% of the FDA recommended maximum daily intake for humans produces anxiety. The anxiety is alleviated by diazepam, a drug used in the treatment of generalized anxiety disorder. We completed RNA sequencing of the amygdala of male mice that were exposed to aspartame or plain drinking water (control), as this brain region regulates anxiety and fear. The aspartame exposure produces changes in the expression of genes regulating excitation-inhibition balance in the amygdala. The anxiety, its response to diazepam and the changes in amygdala gene expression are not limited to the aspartame-exposed individuals but also appear in up to two generations descending from the aspartame-exposed males. Thus, aspartame’s neurobehavioral effects are not limited to those who consume it but also impact generations of descendants, a finding that highlights the need for a re-evaluation of current policies on artificial sweetener use.
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Project description:sucralose administration in mice Raw sequence reads
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Project description:Our previous research demonstrated that caffeine exposure on embryonic day (E) 8.5 increased body weight, altered cardiac morphology and function in adult male mice. However, these adverse effects were not observed in adenosine A1 receptor knockout (A1AR-/-) mice. Our hypothesis is that A1AR action mediates changes in DNA methylation patterns in mice exposed in utero to caffeine and that these changes in methylation lead to long-term effects in adult mice. To test this hypothesis, DNA Methylation 2.1M Deluxe Promoter Arrays (NimbleGen) were used to examine the methylation patterns of DNA isolated from adult left ventricles of the A1AR knockout line exposed to 20 mg/kg caffeine at E8.5 in utero. In A1AR+/+ mice, 4,896 hypermethylated and 2,823 hypomethylated regions were discovered in the left ventricles of the caffeine group compared to the normal saline group. In A1AR-/- mice, 1,024 hypermethylated and 1,757 hypomethylated regions were found in the caffeine group. The differentially methylated regions (DMRs) in the caffeine treated A1AR+/+ hearts mapped to 6,148 genes, 4,853 promoters, 4,111 primary transcripts, 816 CpG islands, and 98 miRNAs. Functional annotation clustering of genes revealed that many genes were involved in the development of hypertrophic cardiomyopathy and other heart diseases, which may explain our earlier findings of thickening of the left ventricular wall after in utero caffeine treatment. The methylation changes in several DMRs, mef2c, ins2, tnnt2, and myh6, were validated by bisulfite sequencing. In summary, in utero caffeine exposure caused DNA methylation changes in adult left ventricles and that these changes may be mediated by A1ARs. Pregnant mice were injected at embryonic day 8.5 with 0.9% NaCl (vehicle) or 20 mg/kg caffeine in vehicle i.p. Pups were born and raised until 8-10 weeks of age. Analysis was performed on the following groups vehicle A1AR+/+ (veh+/+), vehicle A1AR-/- (veh-/-), caffeine A1AR+/+ (caff+/+), and caffeine A1AR-/- (caff-/-). Genomic DNA from left ventricles of adult male mice was used. Two biological replicates were measured for each group.
2015-12-19 | E-GEOD-43030 | biostudies-arrayexpress
Project description:Genetic variants in gene regulatory sequences can modify gene expression and mediate the molecular response to environmental stimuli. In addition, genotype–environment interactions (GxE) contribute to complex traits such as cardiovascular disease. Caffeine is the most widely consumed stimulant and is known to produce a vascular response. To investigate GxE for caffeine, we treated vascular endothelial cells with caffeine and used a massively parallel reporter assay to measure allelic effects on gene regulation for over 43,000 genetic variants. We identified 665 variants with allelic effects on gene regulation and 6 variants that regulate the gene expression response to caffeine (GxE, false discovery rate [FDR] < 5%). When overlapping our GxE results with expression quantitative trait loci colocalized with coronary artery disease and hypertension, we dissected their regulatory mechanisms and showed a modulatory role for caffeine. Our results demonstrate that massively parallel reporter assay is a powerful approach to identify and molecularly characterize GxE in the specific context of caffeine consumption.
2024-02-26 | GSE221514 | GEO
Project description:To screen for xenobiotic-metabolizing-enzyme genes (XME) induced by caffeine exposure, a microarray experiment (performed with a Drosophila pangenomic array (Agilent 4 X 44K) was carried out between control and individuals exposed to caffeine (18mM ). Among 23401 genes consistantly found in the three biological replicates, 13108 showed a significant variation. 749 genes were over-expressed whereas 1518 were under-expressed. Interestingly, several genes belonging to all major classes of detoxification enzymes including XME were among the most highly induced such as CYP12d1, CYP6a8 and CYP6d5. Caffeine ingestion induced gene expression in Drosophila melanogaster male thorax and abdomen was mesured at 12h after exposure to doses of 0, 18mM of caffeine. Three independant experiments were performed at each dose using different drosophila for each experiment.
2014-07-04 | E-GEOD-59084 | biostudies-arrayexpress