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Connecting a Western diet, palmitic acid, and enteric neuropathy
The Journal of Clinical Investigation
|June 1, 2026
Summary
The Western diet’s palmitic acid causes iron-dependent cell death (ferroptosis) in gut neurons, leading to colonic motility loss. Restoring redox balance via NFE2L2 reversed these effects, suggesting a therapeutic target for obesity-related gut disorders.
Area of Science:
- Gastroenterology
- Metabolic Diseases
- Cellular Biology
Background:
- The Western diet (WD) is high in saturated fatty acids like palmitic acid (PA).
- PA is linked to insulin resistance, oxidative stress, inflammation, and organ dysfunction in obesity and diabetes.
- Enteric nervous system (ENS) disorders are common in obesity.
Purpose of the Study:
- To investigate the mechanisms linking WD, PA, ferroptosis, and loss of colonic motility.
- To identify potential therapeutic targets for PA-induced ENS dysfunction.
Main Methods:
- Exposure of murine and human myenteric ganglia to PA.
- Feeding mice a WD for 12 weeks.
- Adeno-associated virus-mediated (AAV-mediated) NFE2L2 overexpression in mice.
Main Results:
- Chronic PA exposure induced ferroptosis in murine and human myenteric ganglia.
- WD-fed mice developed enteropathy and loss of colonic motility.
- NFE2L2 overexpression prevented ferroptosis, restored redox balance, and reversed motility loss.
Conclusions:
- PA-induced ferroptosis is a key mechanism in WD-associated enteropathy and colonic motility loss.
- NFE2L2 acts as a protective factor against PA-induced ENS damage.
- Targeting PA-induced ferroptosis offers a potential therapeutic strategy for obesity-related ENS disorders.
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