Chronic exercise improves hepatic acylcarnitine handling

Diego Hernández-Saavedra, J. Matthew Hinkley, Lisa A. Baer, Kelsey M. Pinckard, Pablo Vidal, Shinsuke Nirengi, Andrea M. Brennan, Emily Y. Chen, Niven R. Narain, Valerie Bussberg, Vladimir V. Tolstikov, Michael A. Kiebish, Christina Markunas, Olga Ilkayeva, Bret H. Goodpaster, Christopher B. Newgard, Laurie J. Goodyear, Paul M. Coen, Kristin I. Stanford

Research output: Contribution to journalArticlepeer-review


Exercise mediates tissue metabolic function through direct and indirect adaptations to acylcarnitine (AC) metabolism, but the exact mechanisms are unclear. We found that circulating medium-chain acylcarnitines (AC) (C12-C16) are lower in active/endurance trained human subjects compared to sedentary controls, and this is correlated with elevated cardiorespiratory fitness and reduced adiposity. In mice, exercise reduced serum AC and increased liver AC, and this was accompanied by a marked increase in expression of genes involved in hepatic AC metabolism and mitochondrial β-oxidation. Primary hepatocytes from high-fat fed, exercise trained mice had increased basal respiration compared to hepatocytes from high-fat fed sedentary mice, which may be attributed to increased Ca2+ cycling and lipid uptake into mitochondria. The addition of specific medium- and long-chain AC to sedentary hepatocytes increased mitochondrial respiration, mirroring the exercise phenotype. These data indicate that AC redistribution is an exercise-induced mechanism to improve hepatic function and metabolism.

Original languageEnglish (US)
Article number109083
Issue number3
StatePublished - Mar 15 2024


  • Cell biology
  • Health sciences
  • Physiology

ASJC Scopus subject areas

  • General


Dive into the research topics of 'Chronic exercise improves hepatic acylcarnitine handling'. Together they form a unique fingerprint.

Cite this