In a rodent model of angiotensin II-accelerated vascular aging, time-restricted feeding preserved intestinal barrier integrity, reshaped the gut microbiome, and raised circulating acetic acid, which in turn reduced arterial stiffness, hypertension, and pathological cardiac remodeling. Fecal transplant reproduced the protection, antibiotic depletion abolished it, and acetate supplementation alone restored it, identifying the metabolite as the causal mediator. Acetate acted through GPR43 to inhibit HDAC3, increase H4K8 acetylation, and block NLRP3-driven pyroptosis and endothelial senescence.
Key Points
- Time-restricted feeding lowered arterial stiffness and reversed cardiac remodeling
- Acetic acid from Limosilactobacillus mediated the entire protective effect
- Acetate blocked NLRP3 pyroptosis and endothelial senescence via GPR43
Longevity Analysis
Meal timing alone, without caloric restriction, altered which bacteria dominated the gut and how much acetate reached the bloodstream — a direct line from eating pattern to vessel wall behavior. The intestinal lining held together better, endotoxin leakage fell, and the low-grade inflammatory signaling that stiffens arteries and drives endothelial cells into senescence quieted. Arterial stiffness and cardiac remodeling are among the more reliable markers of biological age, and this work positions a daily eating window as an upstream lever on both, with a measurable metabolite to track the response.
Original published by Wiley Aging Cell, by Man Liu, Mandi Luo, Yangyang Huang, Tianyi Ji, Yuman Wang, Qian Wang, Jie Huang, Tao Jiang, Cuntai Zhang, Tao Mi, Mian Cheng .