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mitochondrial uncoupling and life extension in mice


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#1 AgeVivo

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Posted 14 August 2010 - 08:55 PM


From memory:
Mitochondrial uncoupling seems to make mice a lot more sportive and agressive, they can run for hours... and possibly live much longer (lifespan experiments would be needed to confirm). It seems their cells work on fat rather than glucose.

#2 AgeVivo

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Posted 14 August 2010 - 09:02 PM

There was a discussion on the subject in the Methuselah Foundation forums, in which Aubrey, Michael, Mark, John had slightly different views, indicative of a not full "non-issue":

http://mfoundation.org/forums/showthread.php?t=979




Hanson RW, Hakimi P., Born to run; the story of the PEPCK-Cmus mouse. Biochimie. 2008 Jun;90(6):838-42:
they lived almost 2 years longer than the controls and had normal litters of pups at 30-35 months of age (most mice stop being reproductively active at 12-18 months). We use the word ‘‘apparent’’ because we have not as yet carried out a detailed aging study, involving multiple mice, which are followed at regular intervals over their lifetime; this type of study is currently in underway in our laboratory
Wow! A high overexpression of PEPCK (linked to use/non-storage of glucose & fat) in skeletal muscles makes these mice hyperactive, eat 60% more than controls, and live much longer !!



Michael makes some valid criticisms of the study, but it is mainly a matter of lack of information. Given how remarkable their limited results are, it would be crazy and very cynical not to want to pursue this further. I think we must all agree that what is needed is for the work to be extended and reproduced with all the proper controls necessary for lifespan studies. Plus, more detailed characterization of what the cellular and physiological changes actually are, right now there is a lot of speculation based and a small amount of data.

Unfortunately, the leader of the lab which generated this mouse doesn't seem to have a strong interest in the potential medical applications. The obvious thing to do is invite him to SENS4 with the intention of encouraging collaborations. Perhaps this will take care of itself before that though, I don't know how far word of this study has spread.


Shortly after Hanson's report, two other groups reported very similar results (hyperphagia, low weight, long lives) from mice with mutations in different genes: PubMed 17962198 and 17662940. It'd be useful to keep these mice in mind too.



#3 AgeVivo

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Posted 14 August 2010 - 09:05 PM

Did we eventually invite the authors to SENS4?
Perhaps it is not too late to invite them to the 10/10/2010 conference in Bruxels????

Richard W. Hanson and Parvin Hakimi
Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, OH 44106–4935
Send correspondence to: Richard W. Hanson, Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland OH 44106–935, Telephone 1-216-368-3880, FAX 1-216-368-4544, E-mail rwh@case.edu
(taken from their free-access article: http://www.ncbi.nlm....96/?tool=pubmed

Edited by AgeVivo, 14 August 2010 - 09:07 PM.





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