A fatty acid produced by the gut bacterium Bacteroides uniformis — pentadecanoic acid (C15:0) — reduced atherosclerotic plaque burden and circulating LDL cholesterol in mice prone to arterial disease. The mechanism runs through the liver: the molecule suppresses hepatic cholesterol synthesis, which activates SREBP2 and upregulates LDL receptors to clear more cholesterol from the blood. Effects were slightly weaker than atorvastatin, and the study measured slowed progression rather than plaque reversal.
Key Points
- Gut-derived C15:0 cut plaque burden roughly 50% in mice
- Effect required functioning hepatic LDL receptors to occur
- Atorvastatin outperformed the bacterial molecule on most endpoints
Longevity Analysis
Cardiovascular risk is increasingly traceable upstream of the liver, to the microbial population that shapes which metabolites reach hepatic tissue in the first place. The same inflammatory signalling that drives plaque-associated macrophage accumulation here links arterial aging to immune activity and intestinal composition, meaning lipid management is not purely a pharmacological question. Human relevance remains unestablished — dosing, delivery, and whether dietary or microbial sources of odd-chain fatty acids reproduce the effect are all open.
Original published by LifeSpan.io, by Arkadi Mazin.