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Open AccessFeature PaperArticle

Chronic High-Fat Diet Induces Early Barrett’s Esophagus in Mice through Lipidome Remodeling

1
QIMR Berghofer Medical Research Institute, Herston, Brisbane, QLD 4006, Australia
2
UQ Diamantina Institute, Faculty of Medicine, The University of Queensland, Woolloongabba, Brisbane, QLD 4072, Australia
3
Envoi Specialist Pathologists, Herston, Brisbane, QLD 4059, Australia
4
Faculty of Medicine, The University of Queensland, Brisbane, QLD 4072, Australia
5
Mater Research Institute, The University of Queensland, Woolloongabba, Brisbane, QLD 4059, Australia
6
Metabolomics Australia, Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, Brisbane, QLD 4072, Australia
7
School of Pharmacy, The University of Queensland, Woolloongabba, Brisbane, QLD 4102, Australia
8
Agilent Technologies, Mulgrave, VIC 3170, Australia
*
Author to whom correspondence should be addressed.
Biomolecules 2020, 10(5), 776; https://doi.org/10.3390/biom10050776
Received: 1 April 2020 / Revised: 7 May 2020 / Accepted: 12 May 2020 / Published: 16 May 2020
(This article belongs to the Special Issue Integrative Multi-Omics in Biomedical Research)
Esophageal adenocarcinoma (EAC) incidence has been rapidly increasing, potentially associated with the prevalence of the risk factors gastroesophageal reflux disease (GERD), obesity, high-fat diet (HFD), and the precursor condition Barrett’s esophagus (BE). EAC development occurs over several years, with stepwise changes of the squamous esophageal epithelium, through cardiac metaplasia, to BE, and then EAC. To establish the roles of GERD and HFD in initiating BE, we developed a dietary intervention model in C57/BL6 mice using experimental HFD and GERD (0.2% deoxycholic acid, DCA, in drinking water), and then analyzed the gastroesophageal junction tissue lipidome and microbiome to reveal potential mechanisms. Chronic (9 months) HFD alone induced esophageal inflammation and metaplasia, the first steps in BE/EAC pathogenesis. While 0.2% deoxycholic acid (DCA) alone had no effect on esophageal morphology, it synergized with HFD to increase inflammation severity and metaplasia length, potentially via increased microbiome diversity. Furthermore, we identify a tissue lipid signature for inflammation and metaplasia, which is characterized by elevated very-long-chain ceramides and reduced lysophospholipids. In summary, we report a non-transgenic mouse model, and a tissue lipid signature for early BE. Validation of the lipid signature in human patient cohorts could pave the way for specific dietary strategies to reduce the risk of BE in high-risk individuals. View Full-Text
Keywords: lipid; lipidomics; cardiac metaplasia; Barrett’s esophagus; esophageal adenocarcinoma; microbiota lipid; lipidomics; cardiac metaplasia; Barrett’s esophagus; esophageal adenocarcinoma; microbiota
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MDPI and ACS Style

Molendijk, J.; Nguyen, T.-M.-T.; Brown, I.; Mohamed, A.; Lim, Y.; Barclay, J.; Hodson, M.P.; Hennessy, T.P.; Krause, L.; Morrison, M.; Hill, M.M. Chronic High-Fat Diet Induces Early Barrett’s Esophagus in Mice through Lipidome Remodeling. Biomolecules 2020, 10, 776. https://doi.org/10.3390/biom10050776

AMA Style

Molendijk J, Nguyen T-M-T, Brown I, Mohamed A, Lim Y, Barclay J, Hodson MP, Hennessy TP, Krause L, Morrison M, Hill MM. Chronic High-Fat Diet Induces Early Barrett’s Esophagus in Mice through Lipidome Remodeling. Biomolecules. 2020; 10(5):776. https://doi.org/10.3390/biom10050776

Chicago/Turabian Style

Molendijk, Jeffrey; Nguyen, Thi-My-Tam; Brown, Ian; Mohamed, Ahmed; Lim, Yenkai; Barclay, Johanna; Hodson, Mark P.; Hennessy, Thomas P.; Krause, Lutz; Morrison, Mark; Hill, Michelle M. 2020. "Chronic High-Fat Diet Induces Early Barrett’s Esophagus in Mice through Lipidome Remodeling" Biomolecules 10, no. 5: 776. https://doi.org/10.3390/biom10050776

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