Abstract
Caloric restriction (CR) has pronounced benefits in promoting healthy aging. Amongst the most frequently implicated physiological mechanisms implicated in this benefit is altered mitochondrial function. Whereas a reduction in mitochondrial reactive oxygen species (ROS) production is a widely consistent effect of CR, an increase in mitochondrial biogenesis, which is accepted by many as fact, is contradicted on several levels, most critically by a lack of increase in mitochondrial protein synthesis rate in vivo. Furthermore, an increase in PGC-1α protein and markers of mitochondrial content with CR is a highly variable observation between studies. On the other hand, deacetylation of several mitochondrial proteins by the sirtuin, Sirt3, is an increasingly reported observation and at least so far, this observation is consistent between studies. Notwithstanding this point, the controversies evident in the published literature underscore the significant questions that remain in our understanding of how CR impacts the mitochondrion and suggest we have yet to fully understand the complexities herein.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.