Hormonal
Inhibition of soluble epoxide hydrolase (sEH) using the inhibitor t-TUCB increases tissue levels of omega-3 epoxides (17,18-EEQ and 19,20-EDP), which reduces inflammation, restores autophagy, and attenuates endoplasmic reticulum stress in obese adipose tissue and liver.
This research suggests that simply consuming omega-3 fatty acids might not be enough for optimal metabolic health in obesity. The body converts these fats into powerful signaling molecules called epoxides, which are normally broken down quickly by an enzyme called sEH. Inhibiting this enzyme (as done with t-TUCB in this study) allows these beneficial signals to persist, reducing liver fat and inflammation. While this specific drug is not a consumer supplement, it highlights the importance of the metabolic pathway of omega-3s and suggests that strategies preserving these epoxides could be therapeutic for metabolic disorders.
In obese fat-1 mice, t-TUCB raised hepatic 17,18-EEQ and 19,20-EDP levels and reinforced the omega-3–dependent reduction observed in tissue inflammation and lipid peroxidation... t-TUCB restored hepatic levels of Atg12-Atg5 and LC3-II conjugates and reduced p62 expression, indicating up-regulation of hepatic autophagy. t-TUCB consistently reduced endoplasmic reticulum stress demonstrated by the attenuation of IRE-1α and eIF2α phosphorylation.
Why this rating
High-quality in vivo animal models (fat-1 mice) with robust mechanistic validation in vitro, though human clinical data is not presented.
Source
Inhibition of soluble epoxide hydrolase modulates inflammation and autophagy in obese adipose tissue and liver: Role for omega-3 epoxides
Cristina López‐Vicario et al. · Proceedings of the National Academy of Sciences · 2014
DOI 10.1073/pnas.1422590112
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