Research
Hormonal
Leptin promotes esophageal adenocarcinoma progression by acting directly on esophageal epithelial cells to increase proliferation, invasiveness, and migration, while reducing apoptosis.
There is no direct practical intervention for leptin levels in this context, but reducing visceral fat may lower circulating leptin levels, potentially reducing this specific pro-tumorigenic signaling.
ModerateSupportsMEDIUM confidence
In vitro studies demonstrate increased proliferation, invasiveness and migration, and reduced programmed cell death among EAC cells treated with leptin.
Why this rating
Based on in vitro studies and rodent models; human clinical data linking circulating leptin directly to EAC progression is less robust than epidemiological links.
Source
Visceral Obesity, Metabolic Syndrome, and Esophageal Adenocarcinoma
Jessie A. Elliott et al. · Frontiers in Oncology · 2021
DOI 10.3389/fonc.2021.627270
narrative_reviewCited 48×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Visceral obesity and metabolic syndrome increase the risk of esophageal adenocarcinoma (EAC) through both GERD-dependent mechanisms (increased acid exposure) and GERD-independent mechanisms (systemic inflammation, adipokine signaling, and microbiome alterations).Good
- Sarcopenic obesity (high BMI with low lean body mass) is associated with increased risk of dose-limiting chemotherapy toxicity and adverse survival outcomes in esophageal cancer patients.Moderate
Related findings · Hormonal
- Initial treatment for type 2 diabetes should be a combination of metformin and either an SGLT-2 inhibitor or a GLP-1 receptor agonist to achieve cardiorenal protection, rather than monotherapy or older agents like sulfonylureas.Strong
- For patients with specific monogenic obesity syndromes (leptin deficiency, POMC/PCSK1/LEPR mutations), targeted pharmacotherapy (recombinant leptin or setmelanotide) is highly effective and should be prioritized, unlike in polygenic obesity.Strong
- Continued weekly administration of 2.4 mg subcutaneous semaglutide prevents weight regain and promotes further weight loss in adults with overweight or obesity, whereas switching to placebo results in significant weight regain.Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →