Summary of Study ST000254
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 PR000206. The data can be accessed directly via it's Project DOI: 10.21228/M8RW2F This work is supported by NIH grant, U2C- DK119886.
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| Study ID | ST000254 |
| Study Title | The role of microbial metabolites in experimental liver disease |
| Study Type | Targeted Metabolomic Analysis of plasma samples |
| Study Summary | Aim 1: Our experimental approach is to understand the effect of drinking water supplemented bacterial metabolite, Indole-3-propionic Acid (IPA), in liver disease in an acute alcohol model. Aim 2: Determine the levels of IPA in plasma of conventional mice in a chronic alcohol model. Aim 3: Determine the levels of IPA in plasma of conventional WT (C57BL/6) and mutant SL (sublytic, which is a mouse with a point mutation in ATP4a) mice. |
| Institute | University of North Carolina |
| Department | Discovery Science Technology |
| Laboratory | Sumner Lab |
| Last Name | Sumner |
| First Name | Susan |
| Address | Eastern Regional Comprehensive Metabolomics Resource Core, UNC Nutrition Research Institute, 500 Laureate Way, Kannapolis, NC, 28081 |
| susan_sumner @unc.edu | |
| Phone | 704-250-5066 |
| Submit Date | 2015-09-29 |
| Num Groups | 2 |
| Total Subjects | 31 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | wiff |
| Uploaded File Size | 8.6 M |
| Analysis Type Detail | LC-MS |
| Release Date | 2016-12-22 |
| Release Version | 1 |
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Project:
| Project ID: | PR000206 |
| Project DOI: | doi: 10.21228/M8RW2F |
| Project Title: | The role of microbial metabolites in experimental liver disease |
| Project Type: | Targeted Metabolomics |
| Project Summary: | Liver fibrosis is the result of chronic liver damage from various etiologies including toxins, alcohol abuse, obesity, or viral hepatitis. Chronic liver disease may progress to cirrhosis, an end stage organ disease, and liver cancer. Patients with chronic liver disease show intestinal bacterial overgrowth and dysbiosis. They also demonstrate increased intestinal permeability, and disease severity correlates with systemic levels of bacterial products. Although experimental liver fibrosis is dependent on gut derived bacterial products, the exact contribution of the commensal microflora to chronic liver disease in unknown. Since the interaction of bacterial products with the innate immune system can also confer protection to the host, we subjected germfree mice to experimental models of liver fibrosis. Results from our laboratory demonstrate that germfree mice show exacerbated liver fibrosis as compared to conventional mice. Our previous studies also have indicated that a bacterial metabolite of tryptophan, Indole-3-propionic Acid (IPA), is absent in germ free mice. In this study we are investigating the role of IPA in acute and chronic models of liver fibrosis. |
| Institute: | University of California, San Diego |
| Last Name: | Schnabl |
| First Name: | Bernd |
| Address: | 9500 Gilman Drive, MC0063 La Jolla, CA 92093 |
| Email: | beschnabl@ucsd.edu |
| Phone: | 858-822-5311 |
