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However, the mechanism by which impaired intestinal synthesis contributes to gut\u2013liver axis aging remains unclear. This study reveals that aging induces a mitochondrial energy crisis and defective membrane localization of ABCA1, significantly inhibiting the biosynthesis of high\u2010density lipoprotein 3 (HDL3) in the intestine. Exogenous supplementation with \u03b2\u2010nicotinamide mononucleotide (NMN) restores intestinal NAD\n                    <jats:sup>+<\/jats:sup>\n                    homeostasis, enhances oxidative phosphorylation efficiency, and promotes ATP\u2010dependent lipid transport, thereby rejuvenating the production of gut\u2010derived HDL3. Further investigations demonstrate that gut\u2010originated HDL3 neutralizes lipopolysaccharide (LPS) in the liver and attenuates TLR4\u2010mediated inflammatory cascades, ultimately ameliorating age\u2010related liver injury. These findings elucidate a novel mechanism whereby NMN modulates the NAD\n                    <jats:sup>+<\/jats:sup>\n                    \u2013mitochondria\u2013ABCA1\u2013HDL3 axis to preserve gut\u2013liver axis function, offering a promising therapeutic strategy for mitigating aging\u2010related pathologies in this metabolic cross\u2010talk.\n                  <\/jats:p>","DOI":"10.1111\/acel.70445","type":"journal-article","created":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T03:35:33Z","timestamp":1773891333000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Aging Triggers an Intestinal Energy Crisis and\n                    <scp>HDL3<\/scp>\n                    Deficiency Disrupting Gut\u2013Liver Axis 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