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Article: Missing Protein and Excercise Inability

Discussion in 'Other Health News and Research' started by leela, Dec 1, 2010.

  1. leela

    leela Slow But Hopeful

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    Couchland, USA
    Interesting implications for PWCs:
    http://www.sciencedaily.com/releases/2010/11/101130122033.htm

    Couch Potato Effect: Missing Protein Leaves Mice Unable to Exercise
    ScienceDaily (Nov. 30, 2010)

    Daniel Kelly, M.D., and his colleagues at Sanford-Burnham Medical Research Institute (Sanford-Burnham) at Lake Nona have unveiled a surprising new model for studying muscle function: the couch potato mouse. While these mice maintain normal activity and body weight, they do not have the energy to exercise. In the December 1 issue of Cell Metabolism, Dr. Kelly's team reports what happens when muscle tissue lacks PGC-1, a protein coactivator that muscles need to convert fuel into energy.

    "Part of our interest in understanding the factors that allow muscles to exercise is the knowledge that whatever this machinery is, it becomes inactive in obesity, aging, diabetes and other chronic conditions that affect mobility," Dr. Kelly explained.

    Normally, physical stimulation boosts PGC-1 activity in muscle cells, which switches on genes that increase fuel storage, ultimately leading to "trained" muscle (the physical condition most people hope to attain through exercise). In obese individuals, PGC-1 levels drop, possibly further reducing a person's capacity to exercise -- creating a vicious cycle. In this study, mice without muscle PGC-1 looked normal and walked around without difficulty, but could not run on a treadmill.
    This is the first time that PGC-1 has been completely removed from muscle tissue, providing researchers with a new model to unravel the protein's role in muscle development, exercise and metabolism. So what happens to mice with muscles short on PGC-1? Their mitochondria -- the part of the cell that converts fuel into energy -- can't function properly, so cells have to work harder to stay vigorous. This extra effort rapidly depletes carbohydrate fuel stores, leading to premature fatigue. In short, PGC-1 is necessary for exercise, but not normal muscle development and activity.

    But these mice held another surprise. PGC-1-deficient couch potato mice were not obese and still respond normally to insulin -- meaning they are not at risk for developing diabetes despite their sedentary lifestyles and mitochondrial problems. This was unexpected because many scientists believe that dysfunctional mitochondria trigger a cascade of insulin resistance and diabetes. This study dispels that notion, instead suggesting that perhaps malfunctioning mitochondria are a result of
    diabetes, rather than a cause.

    "Lo and behold, even though these animals couldn't run, they showed no evidence of insulin resistance," Dr. Kelly said. "We are now investigating what happens when we boost PGC-1 activity intermittently, as normally occurs when a person exercises."
    This work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the National Heart, Lung and Blood Institute (NHLBI), institutes within the National Institutes of Health (NIH), and the American Diabetes Association.
     
  2. George

    George waitin' fer rabbits

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    South Texas
    Can I have the PGC-1 they took out of the mice, please? (big grins) This is a great study though and hopefully lab A is talking to lab B and someone will look at this in the ME/CFS community.
     
  3. pictureofhealth

    pictureofhealth XMRV - L'Agent du Jour

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    Europe
    I sent a copy to ME Research UK (real scientists!) in Scotland, in case it is of interest to them. They fund muscle function and vascular studies and all kinds of ME research. They are also good at communicating with patients.
     
  4. Snow Leopard

    Snow Leopard Senior Member

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    Australia
    The only mention of PGC-1 in a CFS paper that I've found so far:

    http://www.ncbi.nlm.nih.gov/pubmed/18684570

    The paper is not that well written. The first half it reads like a rushed, slighly plagiarized summary of a UK CFS Review article. On the other hand, perhaps it is written like that so that certain UK people actually pay attention.

    The hypothesis is somewhat interesting though.

    http://en.wikipedia.org/wiki/Renin-angiotensin_system

    edit -

    Also: http://www.ncbi.nlm.nih.gov/pubmed/19211721 (vaguely relevant)
     

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