Research Paper Volume 13, Issue 6 pp 7914—7930
A ketogenic diet impacts markers of mitochondrial mass in a tissue specific manner in aged mice
- 1 Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA 95616, USA
- 2 Department of Public Health Sciences, School of Medicine, University of California, Davis, CA 95617, USA
- 3 NIH-West Coast Metabolomics Center, University of California, Davis, CA 95616, USA
- 4 Department of Cell Biology, Physiology and Immunology, Campus de Excelencia Internacional Agroalimentario, ceiA3, University of Córdoba, Córdoba, Spain
- 5 Department of Neurobiology, Physiology, and Behavior, University of California, Davis, CA 95616, USA
Received: November 28, 2020 Accepted: February 16, 2021 Published: March 18, 2021https://doi.org/10.18632/aging.202834
How to Cite
Copyright: © 2021 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Declines in mitochondrial mass are thought to be a hallmark of mammalian aging, and a ketogenic diet (KD) may prevent the age-related decreases in mitochondrial content. The objective of this study was to investigate the impact of a KD on markers of mitochondrial mass. Mice were fed an isocaloric control diet (CD) or KD from 12 months of age. Tissues were collected after 1 month and 14 months of intervention, and a panel of commonly used markers of mitochondrial mass (mitochondrial enzyme activities and levels, mitochondrial to nuclear DNA ratio, and cardiolipin content) were measured. Our results showed that a KD stimulated activities of marker mitochondrial enzymes including citrate synthase, Complex I, and Complex IV in hindlimb muscle in aged mice. KD also increased the activity of citrate synthase and prevented an age-related decrease in Complex IV activity in aged brain. No other markers were increased in these tissues. Furthermore, the impacts of a KD on liver and kidney were mixed with no pattern indicative of a change in mitochondrial mass. In conclusion, results of the present study suggest that a KD induces tissue-specific changes in mitochondrial enzyme activities, or structure, rather than global changes in mitochondrial mass across tissues.