Summary of Study ST003437
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 PR002120. The data can be accessed directly via it's Project DOI: 10.21228/M8KN7C This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
Study ID | ST003437 |
Study Title | White adipose tissue remodeling in Little Brown Myotis (Myotis lucifugus) with white-nose syndrome |
Study Summary | White-nose syndrome (WNS) is a fungal wildlife disease of bats that has caused precipitous declines in certain Nearctic bat species. A key driver of mortality is premature exhaustion of fat reserves, primarily white adipose tissue (WAT), that bats rely on to meet their metabolic needs during winter. However, the pathophysiological and metabolic effects of WNS have remained ill-defined. To elucidate metabolic mechanisms associated with WNS mortality, we infected a WNS susceptible species, the Little Brown Myotis (Myotis lucifugus), with Pseudogymnoascus destructans (Pd) and collected WAT biopsies for histology and targeted lipidomics. These results were compared to the WNS-resistant Big Brown Bat (Eptesicus fuscus). A similar distribution in broad lipid class was observed in both species, with total WAT primarily consisting of triacylglycerides. Baseline differences in WAT chemical composition between species showed that higher glycerophospholipids (GPs) levels in E. fuscus were dominated by unsaturated or monounsaturated moieties and n-6 (18:2, 20:2, 20:3, 20:4) fatty acids. Conversely, higher GP levels in M. lucifugus WAT were primarily compounds containing n-3 (20:5 and 22:5) fatty acids. Following Pd-infection, we found that perturbation to WAT reserves occurs in M. lucifugus, but not in the resistant E. fuscus. A total of 66 GPs (primarily glycerophosphocholines and glycerophosphoethanolamines) were higher in Pd-infected M. lucifugus, indicating perturbation to the WAT structural component. In addition to changes in lipid chemistry, smaller adipocyte sizes and increased extracellular matrix deposition was observed in Pd-infected M. lucifugus. This is the first study to describe WAT GP composition of bats with different susceptibilities to WNS and highlights that recovery from WNS may require repair from adipose remodeling in addition to replenishing depot fat during spring emergence. |
Institute | Georgetown University |
Last Name | Pannkuk |
First Name | Evan |
Address | 3970 Reservoir Rd, NW New Research Build, washington dc, District of Columbia, 20057, USA |
elp44@georgetown.edu | |
Phone | 2026875650 |
Submit Date | 2024-08-20 |
Analysis Type Detail | LC-MS |
Release Date | 2025-01-02 |
Release Version | 1 |
Select appropriate tab below to view additional metadata details:
Project:
Project ID: | PR002120 |
Project DOI: | doi: 10.21228/M8KN7C |
Project Title: | White adipose tissue remodeling in Little Brown Myotis (Myotis lucifugus) with white-nose syndrome |
Project Summary: | White-nose syndrome (WNS) is a fungal wildlife disease of bats that has caused precipitous declines in certain Nearctic bat species. A key driver of mortality is premature exhaustion of fat reserves, primarily white adipose tissue (WAT), that bats rely on to meet their metabolic needs during winter. However, the pathophysiological and metabolic effects of WNS have remained ill-defined. To elucidate metabolic mechanisms associated with WNS mortality, we infected a WNS susceptible species, the Little Brown Myotis (Myotis lucifugus), with Pseudogymnoascus destructans (Pd) and collected WAT biopsies for histology and targeted lipidomics. These results were compared to the WNS-resistant Big Brown Bat (Eptesicus fuscus). A similar distribution in broad lipid class was observed in both species, with total WAT primarily consisting of triacylglycerides. Baseline differences in WAT chemical composition between species showed that higher glycerophospholipids (GPs) levels in E. fuscus were dominated by unsaturated or monounsaturated moieties and n-6 (18:2, 20:2, 20:3, 20:4) fatty acids. Conversely, higher GP levels in M. lucifugus WAT were primarily compounds containing n-3 (20:5 and 22:5) fatty acids. Following Pd-infection, we found that perturbation to WAT reserves occurs in M. lucifugus, but not in the resistant E. fuscus. A total of 66 GPs (primarily glycerophosphocholines and glycerophosphoethanolamines) were higher in Pd-infected M. lucifugus, indicating perturbation to the WAT structural component. In addition to changes in lipid chemistry, smaller adipocyte sizes and increased extracellular matrix deposition was observed in Pd-infected M. lucifugus. This is the first study to describe WAT GP composition of bats with different susceptibilities to WNS and highlights that recovery from WNS may require repair from adipose remodeling in addition to replenishing depot fat during spring emergence. |
Institute: | Georgetown University |
Last Name: | Pannkuk |
First Name: | Evan |
Address: | 3970 Reservoir Rd, NW New Research Build, washington dc, District of Columbia, 20057, USA |
Email: | elp44@georgetown.edu |
Phone: | 2026875650 |
Subject:
Subject ID: | SU003564 |
Subject Type: | Mammal |
Subject Species: | Myotis lucifugus |
Taxonomy ID: | 59463 |
Species Group: | Mammals |
Factors:
Subject type: Mammal; Subject species: Myotis lucifugus (Factor headings shown in green)
mb_sample_id | local_sample_id | Treatment | Sample source |
---|---|---|---|
SA378302 | 1_S_018 | PBST | white adipose tissue |
SA378303 | 1_S_006 | PBST | white adipose tissue |
SA378304 | 1_S_024 | PBST | white adipose tissue |
SA378305 | 1_S_023 | PBST | white adipose tissue |
SA378306 | 1_S_020 | PBST | white adipose tissue |
SA378307 | 1_S_019 | PBST | white adipose tissue |
SA378308 | 1_S_001 | PBST | white adipose tissue |
SA378309 | 1_S_015 | PBST | white adipose tissue |
SA378310 | 1_S_007 | PBST | white adipose tissue |
SA378311 | 1_S_013 | PBST | white adipose tissue |
SA378312 | 1_S_025 | PBST | white adipose tissue |
SA378313 | 1_S_008 | PBST | white adipose tissue |
SA378314 | 1_S_010 | PBST | white adipose tissue |
SA378315 | 1_S_011 | PBST | white adipose tissue |
SA378316 | 2_S_002 | Pd | white adipose tissue |
SA378317 | 2_S_003 | Pd | white adipose tissue |
SA378318 | 2_S_004 | Pd | white adipose tissue |
SA378319 | 2_S_009 | Pd | white adipose tissue |
SA378320 | 2_S_012 | Pd | white adipose tissue |
SA378321 | 2_S_014 | Pd | white adipose tissue |
SA378322 | 2_S_016 | Pd | white adipose tissue |
SA378323 | 2_S_017 | Pd | white adipose tissue |
SA378324 | 2_S_021 | Pd | white adipose tissue |
SA378325 | 2_S_022 | Pd | white adipose tissue |
SA378326 | 2_S_005 | Pd | white adipose tissue |
Showing results 1 to 25 of 25 |
Collection:
Collection ID: | CO003557 |
Collection Summary: | The WAT samples used in this study were collected as part of a captive hibernation experiment performed at Bucknell University from November 2011 to March 2013. The bats were captured between 5 November 2011 and 17 November 2011 in hibernacula in Michigan or Illinois, USA (M. lucifugus) and in Iowa or Illinois, USA (E. fuscus), as previously described (Moore et al. 2018). At the time of capture, none of these populations was known to have previous exposure to WNS. The bats were transported while torpid to Bucknell University in Lewisburg, Pennsylvania, USA where they were treated with either phosphate-buffered saline with 0.5% TWEEN-20 (control) or with a suspension of 350,000 Pd conidia (Pd exposed). Control and treated bats were separately housed in environmental chambers at 4°C and 95% relative humidity with each species in separate enclosures within the chamber. Following 3, 7, or 13 weeks of hibernation, bats were removed from the chamber and humanely euthanized by isoflurane overdose followed by decapitation. For the current study, the analysis was based on disease severity rather than hibernation time and time points were combined. The WAT was dissected from between the pelvis and the skin on both sides of the back, among other tissues, and snap-frozen in liquid nitrogen. Tissues were stored at -80°C to minimize enzymatic activity until they were processed for analysis. |
Sample Type: | Adipose tissue |
Treatment:
Treatment ID: | TR003573 |
Treatment Summary: | The WAT samples used in this study were collected as part of a captive hibernation experiment performed at Bucknell University from November 2011 to March 2013. The bats were captured between 5 November 2011 and 17 November 2011 in hibernacula in Michigan or Illinois, USA (M. lucifugus) and in Iowa or Illinois, USA (E. fuscus), as previously described (Moore et al. 2018). At the time of capture, none of these populations was known to have previous exposure to WNS. The bats were transported while torpid to Bucknell University in Lewisburg, Pennsylvania, USA where they were treated with either phosphate-buffered saline with 0.5% TWEEN-20 (control) or with a suspension of 350,000 Pd conidia (Pd exposed). Control and treated bats were separately housed in environmental chambers at 4°C and 95% relative humidity with each species in separate enclosures within the chamber. Following 3, 7, or 13 weeks of hibernation, bats were removed from the chamber and humanely euthanized by isoflurane overdose followed by decapitation. For the current study, the analysis was based on disease severity rather than hibernation time and time points were combined. The WAT was dissected from between the pelvis and the skin on both sides of the back, among other tissues, and snap-frozen in liquid nitrogen. Tissues were stored at -80°C to minimize enzymatic activity until they were processed for analysis. |
Sample Preparation:
Sampleprep ID: | SP003571 |
Sampleprep Summary: | Briefly, ~10 mg of tissue was homogenized as above, with tissue disruption after a 12-hr period at -80 °C, lipid isolation/purification using a liquid-liquid extraction, and lyophilization. The dried extract was reconstituted in 200 μL of extraction buffer (IPA) and filtered using a 0.2 μM microcentrifuge filter. The supernatant was transferred to MS vial for LC-MS analysis. |
Combined analysis:
Analysis ID | AN005647 | AN005648 |
---|---|---|
Analysis type | MS | MS |
Chromatography type | HILIC | HILIC |
Chromatography system | Shimadzu Nexera X2 | Shimadzu Nexera X2 |
Column | Waters XBridge Amide (100 x 4.6mm,3.5um) | Waters XBridge Amide (100 x 4.6mm,3.5um) |
MS Type | ESI | ESI |
MS instrument type | Triple quadrupole | Triple quadrupole |
MS instrument name | ABI Sciex 5500 QTrap | ABI Sciex 5500 QTrap |
Ion Mode | POSITIVE | NEGATIVE |
Units | peak area | peak area |
Chromatography:
Chromatography ID: | CH004286 |
Chromatography Summary: | Nexera X2 SIL-30 AC auto sampler (Shimazdu) connected with a high flow LC-30AD solvent delivery unit (Shimazdu) and Exion 30AD communication bus module (Shimazdu) |
Instrument Name: | Shimadzu Nexera X2 |
Column Name: | Waters XBridge Amide (100 x 4.6mm,3.5um) |
Column Temperature: | 35 |
Flow Gradient: | The mobile phase was initially 100% solvent A, then a gradient of 3.0 min (solvent A 99.9%, B 0.01%), 3.0 min (solvent A 94%, B 6%), 4.0 min (solvent A 25%, B 75%), 6.0 min (solvent A 0%, B 100%), and then 6.0 min equilibration back to 100% solvent A |
Flow Rate: | 0.7 mL/min |
Solvent A: | 95% acetonitrile/5% water; 10 mM ammonium acetate |
Solvent B: | 50% acetonitrile/50% water; 10 mM ammonium acetate |
Chromatography Type: | HILIC |
Chromatography ID: | CH004287 |
Chromatography Summary: | Nexera X2 SIL-30 AC auto sampler (Shimazdu) connected with a high flow LC-30AD solvent delivery unit (Shimazdu) and Exion 30AD communication bus module (Shimazdu) |
Instrument Name: | Shimadzu Nexera X2 |
Column Name: | Waters XBridge Amide (100 x 4.6mm,3.5um) |
Column Temperature: | 35 |
Flow Gradient: | The mobile phase was initially 100% solvent A, then a gradient of 3.0 min (solvent A 99.9%, B 0.01%), 3.0 min (solvent A 94%, B 6%), 4.0 min (solvent A 25%, B 75%), 6.0 min (solvent A 0%, B 100%), and then 6.0 min equilibration back to 100% solvent A |
Flow Rate: | 0.7 mL/min |
Solvent A: | 95% acetonitrile/5% water; 10 mM ammonium acetate |
Solvent B: | 50% acetonitrile/50% water; 10 mM ammonium acetate |
Chromatography Type: | HILIC |
MS:
MS ID: | MS005371 |
Analysis ID: | AN005647 |
Instrument Name: | ABI Sciex 5500 QTrap |
Instrument Type: | Triple quadrupole |
MS Type: | ESI |
MS Comments: | the qlm file was imported into MultiQuant v 2.0 |
Ion Mode: | POSITIVE |
MS ID: | MS005372 |
Analysis ID: | AN005648 |
Instrument Name: | ABI Sciex 5500 QTrap |
Instrument Type: | Triple quadrupole |
MS Type: | ESI |
MS Comments: | the qlm file was imported into MultiQuant v 2.0 |
Ion Mode: | NEGATIVE |