Visceral Obesity, Metabolic Syndrome, and Esophageal Adenocarcinoma
- PMID: 33777773
- PMCID: PMC7994523
- DOI: 10.3389/fonc.2021.627270
Visceral Obesity, Metabolic Syndrome, and Esophageal Adenocarcinoma
Abstract
Esophageal adenocarcinoma (EAC) represents an exemplar of obesity-associated carcinogenesis, with a progressive increase in EAC risk with increased body mass index. In this context, there is increased focus on visceral adipose tissue and associated metabolic dysfunction, including hypertension, diabetes mellitus and hyperlipidemia, or combinations of these in the metabolic syndrome. Visceral obesity (VO) may promote EAC via both directly impacting on gastro-esophageal reflux disease and Barrett's esophagus, as well as via reflux-independent effects, involving adipokines, growth factors, insulin resistance, and the microbiome. In this review these pathways are explored, including the impact of VO on the tumor microenvironment, and on cancer outcomes. The current evidence-based literature regarding the role of dietary, lifestyle, pharmacologic and surgical interventions to modulate the risk of EAC is explored.
Keywords: Barrett's esophagus; adenocarcinoma; esophageal cancer; gastroesophageal reflux; metabolic syndrome; obesity; tumor microenvironment; visceral obesity.
Copyright © 2021 Elliott and Reynolds.
Conflict of interest statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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