Summary of study ST000048

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 PR000046. The data can be accessed directly via it's Project DOI: 10.21228/M84S36 This work is supported by NIH grant, U2C- DK119886.

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Study IDST000048
Study TitleMetabolomic & lipidomic profiles in response to exogenous insulin & GLP-1 infusions during prolonged fasting (GCMS)
Study TypeTimecourse
Study SummaryThis application requests funding to access state-of-the-art metabolomics and lipidomic platforms at the NIH West Coast Metabolomics Center to analyze plasma samples from recent insulin and glucagon-like peptide-1 (GLP-1) infusion experiments performed in prolong-fasted elephant seals. This suite of studies was designed to better assess the mechanisms contributing to the onset of an insulin resistantlike condition induced by prolonged food deprivation/starvation in mammals. Because elephant seals have evolved robust physiological mechanisms that have allowed them to naturally tolerate such protracted bouts of fasting, they provide an ideal model to address our central hypothesis that increased lipid utilization late in the fast contributes to insulin resistance in elephant seals. Insulin resistance is a common consequence of fasting in mammals and, while the mechanisms by which it manifests are still unclear, a metabolic shift favoring increased mobilization and utilization of lipids during prolonged food deprivation may be a principal causative factor. Insulin resistance has a negative connotation due to its association with obesity and diabetes among humans, but it has been suggested to be an adaptive response to food deprivation.
Institute
University of California, Davis
DepartmentGBSF
LaboratoryWCMC Metabolomics Core
Last NameFiehn
First NameOliver
Address451 Health Sci Drive, Davis, CA 95616
Emailofiehn@ucdavis.edu
Phone1-530-752-8258
Submit Date2014-03-25
Num Groups5
Total Subjects117
Study Comments5 general classes are designed in the experiment:
#1 - A=No GLP1/ Late GTT
#2 - B=GLP1 (Low Dose)
#3 - C=GLP1 (High Dose)
#4 - IL- Early Fasting Insulin Infusion
#5 - IE- Late Fasting Insulin Infusion
Each of the 5 classes has 6 timepoints (5x6):
T1 - 0 min
T2 - 10 min
T3 - 30 min
T4 - 60 min
T5 - 120 min
Each timepoint had 5 animals (5 animals x 5 classes x 6 timepoints = 150 total
Because certain animals and timepoints had to be excluded 108 measurments remain.
The experiment also contains 9 technical replicates of pooled samples (pool)
The total sample number is 108 (biological) + 9 pooled samples = 117
Raw Data AvailableYes
Raw Data File Type(s).cdf, .peG,.txt
Uploaded File Size1.8 G
Analysis Type DetailGC-MS
Release Date2014-04-24
Release Version1
Oliver Fiehn Oliver Fiehn
https://dx.doi.org/10.21228/M84S36
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000046
Project DOI:doi: 10.21228/M84S36
Project Title:Metabolomic & lipidomic profiles in response to exogenous insulin & GLP-1 infusions during prolonged fasting
Project Type:Timecourse
Project Summary:This application requests funding to access state-of-the-art metabolomics and lipidomic platforms at the NIH West Coast Metabolomics Center to analyze plasma samples from recent insulin and glucagon-like peptide-1 (GLP-1) infusion experiments performed in prolong-fasted elephant seals. This suite of studies was designed to better assess the mechanisms contributing to the onset of an insulin resistantlike condition induced by prolonged food deprivation/starvation in mammals. Because elephant seals have evolved robust physiological mechanisms that have allowed them to naturally tolerate such protracted bouts of fasting, they provide an ideal model to address our central hypothesis that increased lipid utilization late in the fast contributes to insulin resistance in elephant seals. Insulin resistance is a common consequence of fasting in mammals and, while the mechanisms by which it manifests are still unclear, a metabolic shift favoring increased mobilization and utilization of lipids during prolonged food deprivation may be a principal causative factor. Insulin resistance has a negative connotation due to its association with obesity and diabetes among humans, but it has been suggested to be an adaptive response to food deprivation.
Institute:University of California, Merced
Department:School of Natural Sciences
Laboratory:Molecular and Cellular Biology, Natural Sciences
Last Name:Ortiz
First Name:Rudy
Address:5200 N. Lake Rd.; Merced, CA 95343
Email:rortiz@ucmerced.edu
Phone:209.228.2964
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