Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA394124 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Consumers are exposed through food intake to a cocktail of pesticides at low doses. Epidemiological evidence suggested a link between pesticide exposure and the development of the metabolic syndrome. We used a mouse model to mimic consumer exposure and assessed the metabolic consequences of a chronic dietary exposure to a cocktail of 6 commonly used pesticides (boscalid, captan, chlorpyrifos, thiofanate, thiacloprid and ziram) at non-toxic doses (acceptable daily intake ADI). One year of exposure induced body weight and adiposity gain, hepatic steatosis and glucose intolerance in males. Females did not display significant changes in body weight but displayed fasted hyperglycemia and perturbations of gut-microbiota related urinary metabolites. Exposure of mice invalidated for the constitutive androstane receptor (CAR) demonstrated that this nuclear receptor was involved in the observed sexual dimorphic response to pesticide exposure. These results demonstrate for the first time that chronic dietary exposure to a pesticide cocktail at the ADI levels induces metabolic perturbations favouring obesity and diabetic state and raise the questions of the relevance of the ADI levels of individual pesticides when present in mixture.
2018-07-05 | GSE101405 | GEO
Project description:Human health effects from chronic exposure to pesticide residues are little investigated. We compared standard histopathology and serum biochemistry measures and multi-omics analyses in an in vivo subchronic toxicity test of a glyphosate, its formulated product MON 52276, and mixture of six pesticide active ingredients frequently detected in foodstuffs (azoxystrobin, boscalid, chlorpyrifos, glyphosate, imidacloprid and thiabendazole). Sprague-Dawley rats were administered with the pesticide mixture with each ingredient at its regulatory permitted acceptable daily intake.
2021-04-12 | GSE157551 | GEO
Project description:Human health effects from chronic exposure to pesticide residues are little investigated. We compared standard histopathology and serum biochemistry measures and multi-omics analyses in an in vivo subchronic toxicity test of a glyphosate, its formulated product MON 52276, and mixture of six pesticide active ingredients frequently detected in foodstuffs (azoxystrobin, boscalid, chlorpyrifos, glyphosate, imidacloprid and thiabendazole). Sprague-Dawley rats were administered with the pesticide mixture with each ingredient at its regulatory permitted acceptable daily intake.
2021-04-12 | GSE157426 | GEO
Project description:<div>BACKGROUND: Epidemiological evidence suggests a link between pesticide exposure and the development of metabolic diseases. However, most experimental studies have evaluated the metabolic effects of pesticides using individual molecules, often at non-relevant doses or in combination with other risk factors such as high fat diets.<br></div><div>OBJECTIVES: We aimed to evaluate, in mice, the metabolic consequences of chronic dietary exposure to a pesticide mixture at non-toxic doses, relevant to consumers’ risk assessment.<br></div>METHODS: A mixture of six pesticides commonly used in France i.e. boscalid, captan, chlorpyrifos, thiofanate, thiacloprid, and ziram was incorporated in a standard chow diet, at doses exposing mice to the acceptable daily intake (ADI) of each pesticide. Wild-type (WT) and Constitutive Androstane Receptor knock-out (CAR-/-) C57Bl6/J male and female mice were exposed for 52 weeks. We assessed metabolic parameters (body-weight, food and water consumption, glucose tolerance, urinary metabolome) throughout the experiment. At the end of the experiment, we evaluated liver metabolism (histology, transcriptomics, metabolomics) and pesticide detoxification using LC/MS.<br>RESULTS: In males, pesticide exposure increased body weight and adiposity and induced hepatic steatosis and glucose intolerance. Exposed females exhibited fasted hyperglycaemia, hepatic oxidative stress and perturbations of gut microbiota-related urinary metabolites. The Constitutive Androstane Receptor is involved in the sexually dimorphic response to pesticide exposure.<br><div> CONCLUSIONS: We show for the first time the sexually dimorphic obesogen and diabetogen effects of a chronic dietary exposure <br>to a realistic mixture of pesticides, which are partially mediated through CAR. This raises questions about the relevance of ADI for <br>individual pesticides when present in a mixture.</div><div><br></div><div><b>Untargeted urine, plasma and liver NMR assay</b> protocols and data are reported in the current study <b>MTBLS602</b>.<br><br><b>Untargeted urine UPLC-MS assay</b> protocols and data associated to this study are reported in <a href="https://www.ebi.ac.uk/metabolights/MTBLS596"><b>MTBLS596</b></a>.<br></div><div><br></div>
2018-05-01 | MTBLS602 | MetaboLights
Project description:<div>BACKGROUND: Epidemiological evidence suggests a link between pesticide exposure and the development of metabolic diseases. However, most experimental studies have evaluated the metabolic effects of pesticides using individual molecules, often at non relevant doses or in combination with other risk factors such as high fat diets.<br></div><div>OBJECTIVES: We aimed to evaluate, in mice, the metabolic consequences of chronic dietary exposure to a pesticide mixture at non-toxic doses, relevant to consumers’ risk assessment.<br></div> METHODS: A mixture of six pesticides commonly used in France i.e. boscalid, captan, chlorpyrifos, thiofanate, thiacloprid, and ziram was incorporated in a standard chow diet, at doses exposing mice to the acceptable daily intake (ADI) of each pesticide. Wild-type (WT) and Constitutive Androstane Receptor knock-out (CAR-/-) C57Bl6/J male and female mice were exposed for 52 weeks. We assessed metabolic parameters (body-weight, food and water consumption, glucose tolerance, urinary metabolome) throughout the experiment. At the end of the experiment, we evaluated liver metabolism (histology, transcriptomics, metabolomics) and pesticide detoxification using LC/MS.<br>RESULTS: In males, pesticide exposure increased body weight and adiposity and induced hepatic steatosis and glucose intolerance. Exposed females exhibited fasted hyperglycaemia, hepatic oxidative stress and perturbations of gut microbiota-related urinary metabolites. The Constitutive Androstane Receptor is involved in the sexually dimorphic response to pesticide exposure.<br><div> CONCLUSIONS: We show for the first time the sexually dimorphic obesogen and diabetogen effects of a chronic dietary exposure to a realistic mixture of pesticides, which are partially mediated through CAR. This raises questions about the relevance of ADI for individual pesticides when present in a mixture.</div><div><br></div><div><b>Untargeted urine UPLC-MS assay</b> protocols and data are reported in the current study <b>MTBLS596</b>.</div><div><br><b>Untargeted urine, plasma and liver NMR assay</b> protocols and data associated to this study are reported in <a href=https://www.ebi.ac.uk/metabolights/mtbls602><b>MTBLS602</b></a>.<br></div>
2019-05-28 | MTBLS596 | MetaboLights
Project description:Obesity is a major contributor to metabolic and cardiovascular diseases. Senescence is a highly dynamic process activated by diverse stimuli and increased cellular senescence has been associated with age-related disorders. Here, we investigated the impact of cellular senescence in obesogenic diet-related metabolic and cardiac dysfunctions. An obesogenic diet induced an increase on body weight gain and adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hepatic disorders in mice; however, these alterations were prevented by a senolytic cocktail (dasatinib and quercetin), which leads to removal of senescent cells. In addition, the elimination of senescent cells counteracted the activation of the senescent program and DNA damage in the white adipose tissue (WAT) induced by an obesogenic diet. Obese mice had an increase of the senescence-associated secretory phenotype (SASP) and DNA damage in the heart, cardiac hypertrophy, and diastolic dysfunction; however, the use of a senolytic combination abolished these myocardial alterations caused by an obesogenic diet. Transcriptomic analysis of the hearts revealed that obese mice exhibited a downregulation of genes associated with fatty acid metabolism, oxidative phosphorylation, PI3K AKT MTOR signaling, P53 pathway, and DNA repair; however, the treatment with senolytic cocktail induced an increase of these pathways in the heart. Collectively, these data suggest that obesogenic diet elicits WAT and cardiac senescence program in mice, and that targeting senescent cells may be a novel therapeutic strategy for attenuating obesity-related metabolic and cardiac disorders.
2024-12-19 | GSE264313 | GEO
Project description:Quantitative mass spectrometry reveals food intake-induced neuropeptide level change in rat brain and functional assessment of selected neuropeptides as feeding regulators
2016-08-30 | MSV000080106 | MassIVE
Project description:Interventions: An intervention period: The glucide diet is three months by every meal. A daily glucide intake: Less than 5% of intake energy. Daily EPA(eicosapentaenoic acid) intake: More than 2 g. A daily protein intake: More than weight * 1.6g. A daily middle chain fatty acid intake: More than 40 g.
Primary outcome(s): The evaluation is every month after a glucide diet start. Blood sugar level, blood ketone body density, the weight, albumin level, renal function (BUN, Cr), liver function (GOT, GPT), QOL score)
Study Design: Single arm Non-randomized
| 2644712 | ecrin-mdr-crc