In mice, daily supplementation with the short-chain fatty acid butyrate, begun at 18 months (roughly equivalent to late middle age in humans), extended survival in both sexes. Treated animals showed lower adiposity and fasting glucose, better physical performance, and attenuated cardiac hypertrophy, fibrosis, and systolic and diastolic dysfunction. Proteomics and RNA sequencing pointed to remodeled extracellular-matrix, lipid-metabolism, and autophagy programs, alongside healthier mitochondrial structure and respiration. Butyrate's benefits for left-ventricular hypertrophy and diastolic function disappeared without the autophagy gene ATG7. These findings come from animals, not humans. Butyrate is the fiber-fermentation product of gut bacteria, so the work feeds a growing case that microbiome-derived metabolites influence aging, but translation is far from guaranteed. Starting treatment late is the study's strongest feature, since few interventions are tested after aging is well underway, and the ATG7 dependence offers a credible mechanism rather than a correlation. Open questions remain: dose and delivery route matter, as oral butyrate is largely absorbed in the gut and may not reach the heart at meaningful levels in people, and human trials of butyrate for cardiometabolic outcomes are small and short. Mouse lifespan gains frequently fail to transfer to humans. This is a preprint that has not undergone peer review, so survival statistics and mechanistic claims may shift under scrutiny. Overall, a promising but preclinical result that strengthens the autophagy-aging link without justifying supplementation on its own.