07 Jun Metformin May Extend Lifespan By Increasing Reactive Oxygen Species

MedicalResearch.com Interview with:
Wouter De Haes
Functional Genomics and Proteomics (Schoofs lab)
Zoological Institute
Leuven Belgium

MedicalResearch: What are the main findings of the study?

Answer: We discovered that the lifespan-extending effect of metformin is dependent on the increased production of reactive oxygen species in the roundworm Caenorhabditis elegans. Antioxidants, compounds that remove these reactive oxygen species, abolished the lifespan-extending effect of metformin, adding to the growing body of evidence that anti-oxidants are not as beneficial for health as generally assumed. We also identified the protein, belonging to the group of peroxiredoxins, that seems responsible for translating this increase in reactive oxygen species production into longevity.

MedicalResearch: Were any of the findings unexpected?

Answer: Yes, we did not, at first, expect that metformin would increase the production of reactive oxygen species, as these were once thought to be the culprit of ageing.

MedicalResearch: What should clinicians and patients take away from your report?

Answer: Fundamental research in model organisms such as C. elegans can be helpful in uncovering the mechanisms underlying healthy ageing. While one should be careful not to over-extrapolate findings from model organisms to humans, the study is promising as a foundation for future research. As such, more time will be needed before patients will benefit from this study.

MedicalResearch: What recommendations do you have for future research as a result of this study?

Answer: I’d recommend more research into the exact workings of peroxiredoxins, the proteins responsible for translating the reactive oxygen species signal into longevity. Understanding how organisms control the ageing process, and how activation of peroxiredoxins leads to an increase in healthy lifespan, may lead to more targeted interventions in the future.

Citation:

Metformin promotes lifespan through mitohormesis via the peroxiredoxin PRDX-2
Wouter De Haes, Lotte Frooninckx, Roel Van Assche, Arne Smolders, Geert Depuydt, Johan Billen, Bart P. Braeckman, Liliane Schoofs, and Liesbet Temmerman

PNAS 2014 ; published ahead of print June 2, 2014, doi:10.1073/pnas.1321776111

Last Updated on June 7, 2014 by Marie Benz MD FAAD