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..defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity.., 2020, Choi et al

Discussion in 'Health News and Research unrelated to ME/CFS' started by Andy, Jan 13, 2020.

  1. Andy

    Andy Committee Member & Outreach

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    Full title - An adipocyte-specific defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity in mouse models
    Paywall, https://link.springer.com/article/10.1007/s00125-019-05082-7
    Sci hub, https://sci-hub.se/10.1007/s00125-019-05082-7
     
    ukxmrv, Hutan, spinoza577 and 2 others like this.
  2. Hutan

    Hutan Moderator Staff Member

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    Thinking aloud here, do join in/correct me if you feel like it.

    Mitochondrial oxidative phosphorylation (Oxphos) is the production of ATP in mitochondria; it uses oxygen. (Whereas glycolysis happens in the cytoplasm (in the cell but outside the mitochondria) and doesn't use oxygen).

    So these researchers have gene knock-out mice that have reduced Oxphos in their adipocytes (adipocytes = essentially, fat cells). And that's interesting because people with ME seem to have reduced Oxphos, especially when in PEM. I think we swap to glycolysis quicker than healthy people during a CPET (and quicker again in another CPET the following day).

    They also did an in vitro analysis -
    So doxycycline decreased OxPhos in fat cells! and also initiates the mitochondrial unfolded protein response. Maybe it does that in other cells too? (I wonder, could extended courses of doxycycline for malaria prophylaxis be harmful in some people?)


    That's interesting because Nacul et al found
    (although there was speculation that the GDF15 was inversely related to activity levels).

     
    Caesar and Andy like this.

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