Summary of Study ST002161
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 PR001374. The data can be accessed directly via it's Project DOI: 10.21228/M84127 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
Study ID | ST002161 |
Study Title | Glycerate Production from Intestinal Fructose Metabolism Elevated by Dietary Fat Induces Glucose Intolerance Through β-cell Damage |
Study Summary | Dietary fructose, especially in the context of a high-fat western diet, has been linked to type 2 diabetes. Although the effect of fructose on liver metabolism has been extensively studied, a significant portion of the fructose is first metabolized in the small intestine. Here we report that dietary fat enhances intestinal fructose metabolism, which releases glycerate into the blood. High systemic glycerate levels reduce pancreatic islet sizes and β-cell content, thus inducing glucose intolerance. Our findings provide an additional link between dietary fructose and diabetes that is modulated by dietary fat. |
Institute | Duke University |
Last Name | Wong |
First Name | Chi Wut |
Address | CEIMAS, 101 Science Dr. Room 2141, Durham, NC, 27709, USA |
chiwut.wong@duke.edu | |
Phone | 9495290320 |
Submit Date | 2022-05-11 |
Raw Data Available | Yes |
Raw Data File Type(s) | mzXML |
Analysis Type Detail | LC-MS |
Release Date | 2022-07-06 |
Release Version | 1 |
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Project:
Project ID: | PR001374 |
Project DOI: | doi: 10.21228/M84127 |
Project Title: | Glycerate Production from Intestinal Fructose Metabolism Elevated by Dietary Fat Induces Glucose Intolerance Through β-cell Damage |
Project Summary: | Dietary fructose, especially in the context of a high-fat western diet, has been linked to type 2 diabetes. Although the effect of fructose on liver metabolism has been extensively studied, a significant portion of the fructose is first metabolized in the small intestine. Here we report that dietary fat enhances intestinal fructose metabolism, which releases glycerate into the blood. High systemic glycerate levels reduce pancreatic islet sizes and β-cell content, thus inducing glucose intolerance. Our findings provide an additional link between dietary fructose and diabetes that is modulated by dietary fat. |
Institute: | Duke University |
Last Name: | Wong |
First Name: | Chi Wut |
Address: | CEIMAS, 101 Science Dr. Room 2141, Durham, NC, 27709, USA |
Email: | chiwut.wong@duke.edu |
Phone: | 9495290320 |