Summary of Study ST003522

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 PR002137. The data can be accessed directly via it's Project DOI: 10.21228/M8CZ33 This work is supported by NIH grant, U2C- DK119886.

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Study IDST003522
Study TitleUntargeted mass spectrometry analysis of neutral lipids in MC38 tumors and visceral adipose tissues of control-diet and high fat diet-fed C57BL/6 mice
Study SummaryBoth tumors and the visceral adipose tissues were collected from Control Diet (CD) and High Fat Diet (HFD)-fed C57BL/6 (B6) mice. Mice were fed a HFD for 2 months. For tumor studies, MC38 tumors were subcutaneously injected after 2 months of feeding mice the HFD. Tumors were allowed to grow for 3 weeks, at which point, tumors from CD and HFD-fed mice were harvested and snap frozen. Visceral adipose tissues were also collected from these mice and snap frozen. Subsequently, samples were sent to the UC Davis Metabolomics Core for analysis of neutral lipids. Some triglycerides, including TG(54:3), were found to be significantly more abundant in the adipose tissue and tumors of HFD-fed mice compared to CD-fed mice.
Institute
Stanford University
Last NameEngleman
First NameEdgar
Address3373 Hillview Avenue
Emailsbagchi@stanford.edu
Phone4086214773
Submit Date2024-09-24
Analysis Type DetailLC-MS
Release Date2024-12-02
Release Version1
Edgar Engleman Edgar Engleman
https://dx.doi.org/10.21228/M8CZ33
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR002137
Project DOI:doi: 10.21228/M8CZ33
Project Title:Acid-sensing receptor, GPR65, on tumor macrophages drives accelerated tumor growth in obesity
Project Summary:Multiple cancers, including colorectal cancer (CRC), are more frequent and often more aggressive in obese individuals. Here, we show that macrophages accumulate within tumors of obese CRC patients and in obese CRC mice and promote accelerated tumor growth. These changes are initiated by oleic acid accumulation and subsequent tumor cell-derived acid production, and driven by signaling through GPR65, an acid-sensing receptor on CRC-associated macrophages. We demonstrate a similar role for GPR65 in hepatocellular carcinoma (HCC) in obese mice. Tumors in obese patients with CRC or HCC also exhibit increased GPR65 expression, suggesting that the mechanism revealed here likely contributes to tumor growth in a range of obesity-associated cancers and represents a potential therapeutic target.
Institute:Stanford University
Last Name:Bagchi
First Name:Sreya
Address:3373 Hillview Avenue
Email:sbagchi@stanford.edu
Phone:4086214773

Subject:

Subject ID:SU003651
Subject Type:Mammal
Subject Species:Mus musculus
Taxonomy ID:10090
Species Group:Mammals

Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Diet Sample source
SA386784CD5CD MC38 murine colorectal tumor
SA386785CD2CD MC38 murine colorectal tumor
SA386786CD1CD MC38 murine colorectal tumor
SA386787CD4CD MC38 murine colorectal tumor
SA386788CD3CD MC38 murine colorectal tumor
SA386789CD10CD Visceral adipose tissue
SA386790CD9CD Visceral adipose tissue
SA386791CD7CD Visceral adipose tissue
SA386792CD8CD Visceral adipose tissue
SA386793CD6CD Visceral adipose tissue
SA386794HFD5HFD MC38 murine colorectal tumor
SA386795HFD4HFD MC38 murine colorectal tumor
SA386796HFD1HFD MC38 murine colorectal tumor
SA386797HFD3HFD MC38 murine colorectal tumor
SA386798HFD2HFD MC38 murine colorectal tumor
SA386799HFD6HFD Visceral adipose tissue
SA386800HFD7HFD Visceral adipose tissue
SA386801HFD8HFD Visceral adipose tissue
SA386802HFD9HFD Visceral adipose tissue
SA386803HFD10HFD Visceral adipose tissue
Showing results 1 to 20 of 20

Collection:

Collection ID:CO003644
Collection Summary:MC38 tumors and visceral adipose tissues from CD and HFD-fed mice were collected 3 weeks post tumor implantation. MC38 tumors were subcutaneously injected after 2 months of feeding mice the HFD. Tumors were allowed to grow for 3 weeks, at which point, tumors from CD and HFD-fed mice were harvested and snap frozen. Visceral adipose tissues were also collected from these mice and snap frozen.
Sample Type:Whole tumor, Visceral adipose tissue

Treatment:

Treatment ID:TR003660
Treatment Summary:Mice were fed either CD or HFD for two months.

Sample Preparation:

Sampleprep ID:SP003658
Sampleprep Summary:Both tumors and visceral adipose tissues were isolated from the mice and immediately snap frozen in liquid nitrogen. Subsequently, they were sent for analysis to the UC Davis Metabolomics Core.
Sampleprep Protocol Filename:Fiehn_laboratory_Lipidomics_Protocol.pdf

Chromatography:

Chromatography ID:CH004390
Methods Filename:Fiehn_laboratory_Lipidomics_Protocol.pdf
Instrument Name:Agilent 1290 Infinity
Column Name:Waters ACQUITY UPLC CSH C18 (100 x 2.1mm,1.7um)
Column Temperature:65°C
Flow Gradient:0 min 15% (B), 0–2 min 30% (B), 2–2.5 min 48% (B), 2.5–11 min 82% (B), 11–11.5 min 99% (B), 11.5–12 min 99% (B), 12–12.1 min 15% (B), 12.1–15 min 15% (B)
Flow Rate:0.6 mL/min
Solvent A:60% acetonitrile/40% water; 10 mM ammonium formate; 0.1% formic acid
Solvent B:90% isopropanol/10% acetonitrile; 10 mM ammonium formate; 0.1% formic acid
Chromatography Type:Reversed phase

Analysis:

Analysis ID:AN005784
Analysis Type:MS
Analysis Protocol File:Fiehn_laboratory_Lipidomics_Protocol.pdf
Chromatography ID:CH004390
Num Factors:4
Num Metabolites:96
Rt Units:Minutes
Units:Relative peak intensity
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