Summary of Study ST001145
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 PR000765. The data can be accessed directly via it's Project DOI: 10.21228/M8SQ4S 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 | ST001145 |
| Study Title | UPLC-MS Analysis of Lipids From Insulin Resistant Femoral Muscles of Diet-induced Obese Mice |
| Study Type | Lipidomics, Basic Research |
| Study Summary | Muscle insulin resistance is a fundamental contributor in the pathogenesis of obesity-related diseases like type 2 diabetes. Increased triglyceride concentration in muscle tissue, as seen with obesity, is associated with inhibition of insulin action and decreased glucose uptake. Here we use liquid chromatography paired with mass spectrometry (LCMS) to identify patterns of lipid species in femoral muscle of mice associated with diet-induced insulin resistance. Mice were fed a standard CHOW diet for 5 weeks or HFD for 5 or 13 weeks. 806 lipids were significantly different (p ≤ 0.05) between HFD-induced insulin resistant muscle and CHOW insulin sensitive. Of these 217 lipid species were quantified and annotated based on principle components analysis, significance (p ≤ 0.01) and fold change of relative abundance values. CHOW insulin sensitive muscle was associated with triglycerides and phospholipids that contained higher abundance of long-chain highly unsaturated fatty acids. Serine and inositol phospholipids favored insulin sensitive femoral muscle, yet higher abundance also occurred in 13 week HFD mice compared with 5 week. Consequently, phospholipid imbalance may be indicative of cell membrane dysfunction. HFD insulin resistant femoral muscle contained triglycerides with less carbons, compared with CHOW, which were predominantly saturated. In addition, there was greater abundance of diacylglycerides and sphingomyelin, but not ceramides. Extending HFD intake to 13 weeks did not cause increased abundance of deleterious lipids with the exception of sphingomyelin. Overall, distinct lipid combinations, perhaps even ratios, should be characterized when identifying what contributes to the maintenance or dysregulation of muscle insulin sensitivity. |
| Institute | Colorado State University |
| Department | Food Science and Human Nutrition |
| Laboratory | Adipose Tissue |
| Last Name | Foster |
| First Name | Michelle |
| Address | 1571 Campus Delivery, Fort Collins, Colorado 80523 |
| Michelle.Foster@colostate.edu | |
| Phone | 9704916189 |
| Submit Date | 2019-01-18 |
| Num Groups | 3 |
| Total Subjects | 21 |
| Num Males | 21 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | cdf |
| Analysis Type Detail | LC-MS |
| Release Date | 2020-01-06 |
| Release Version | 1 |
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Treatment:
| Treatment ID: | TR001225 |
| Treatment Summary: | Male C57BL/6 mice, 3 months of age, (Jackson Laboratory, Bar Harbor, Maine) were allowed to acclimate for one week before experiment start. Mice were individually housed under controlled conditions (12:12 light-dark cycle, 50–60% humidity, and 25° C) and had ad libitum access to standard CHOW diet (Envigo Teklad 6% fat 7002, Madison, WI). Lipids in the CHOW diet consisted of an assortment of fatty acids where linoleic > oleic > palmitic > linolenic > stearic. Following a baseline glucose tolerance test (GTT), mice were grouped according to mean GTT and body mass into a standard 5 week CHOW (n = 10) or Western (HFD; high-fat, high-sugar; 21% milk fat and 34% sucrose (Envigo TD.08811); 5 (n = 5) and 13 week (n = 6)) diet group. The saturated fatty acids in HFD ranged from 4:0 to 18:0, however, palmitate (16:0) followed by steric (18:0) and myristic (14;0) where highest in quantity. |
| Treatment: | Diet |
| Treatment Compound: | Envigo TD.08811 |
| Treatment Route: | oral |
