Summary of project PR001717
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001717. The data can be accessed directly via it's Project DOI: 10.21228/M8RX4J This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR001717 |
| Project DOI: | doi: 10.21228/M8RX4J |
| Project Title: | Prj171_Mm_TCDD_RDDR-28D_Male |
| Project Type: | targeted metabolomics |
| Project Summary: | The aryl hydrocarbon receptor (AhR) is a transcription factor activated by structurally diverse chemicals, endogenous metabolites, and natural products. AhR activation causes the dissociation of chaperone proteins, followed by translocation to the nucleus and dimerization with the AhR nuclear translocator (ARNT). The complex binds dioxin response elements (DREs; 5’-GCGTG-3’) eliciting changes in gene expression. AhR activation by its most potent ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) promotes the development and progression of non-alcoholic fatty liver disease (NAFLD). NAFLD is a spectrum of pathologies that spans simple, reversible, and benign lipid accumulation (hepatic steatosis), to steatosis with inflammation (steatohepatitis) and collagen deposition (fibrosis/cirrhosis) in the absence of excessive alcohol consumption. NAFLD prevalence is projected to increase from ~83 million in 2015 to ~101 million by 2030 in the US alone, while increasing the risk for more complex disorders including Metabolic Syndrome, cardiovascular disease, diabetes, cirrhosis, end-stage liver disease and hepatocellular carcinoma (HCC). The role of AhR-mediated metabolic dysregulation in hepatotoxicity and the etiology of more complex metabolic diseases warrants further investigation. Therofore, in this project on PND28 mice were orally gavaged at the start of the light cycle (zeitgeber [ZT] 0-1) with 0.1 ml sesame oil vehicle or 0.01, 0.03, 0.1, 0.3, 1, 3, 10, and 30 ug/kg body weight TCDD every 4 days for 28 days for a total of 7 treatments. The first gavage was administered on day 0, with the last gavage administered on day 24 of the 28-day study. On day 28, tissue samples were harvested (ZT 0-3), immediately flash frozen in liquid nitrogen and stored at -80°C until analysis. |
| Institute: | Michigan State University |
| Department: | Biochemistry and Molecular Biology |
| Last Name: | Zacharewski |
| First Name: | Timothy |
| Address: | 48824:East Lansing |
| Email: | tzachare@msu.edu |
| Phone: | 517-884-2054 |
| Funding Source: | NIEHS; Superfund Basic Research Program R01ES029541:P42ES004911 |
Summary of all studies in project PR001717
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST002756 | Prj171_Mm_TCDD_RDDR-28D_Male | Mus musculus | Michigan State University | MS | 2023-07-14 | 1 | 30 | Uploaded data (6.6M)* |
| ST003529 | Measurement of itaconic acid in liver of male mice treated with TCDD | Mus musculus | Michigan State University | MS | 2024-11-04 | 1 | 20 | Uploaded data (733.6M)* |
