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    This experiment tested the effects of nicotinamide mononucleotide (NMN), a precursor of NAD+, on mouse metabolism and aging. Mice who did not receive NMN showed declining levels of NAD+, ATP, and COX as they aged. Mice who received NMN saw increases in these levels and improvements to skeletal muscle metabolism. However, longer treatments may be needed to fully reverse aging effects and increase lifespan, as muscle strength was not improved after just one week of treatment. While promising, more research is needed to understand the genetic factors and potential human applications of NMN supplements.

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    Nad Paper Needs Citations

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    This experiment tested the effects of nicotinamide mononucleotide (NMN), a precursor of NAD+, on mouse metabolism and aging. Mice who did not receive NMN showed declining levels of NAD+, ATP, and COX as they aged. Mice who received NMN saw increases in these levels and improvements to skeletal muscle metabolism. However, longer treatments may be needed to fully reverse aging effects and increase lifespan, as muscle strength was not improved after just one week of treatment. While promising, more research is needed to understand the genetic factors and potential human applications of NMN supplements.

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    This experiment tested the effects of nicotinamide mononucleotide (NMN), a precursor of NAD+, on mouse metabolism and aging. Mice who did not receive NMN showed declining levels of NAD+, ATP, and COX as they aged. Mice who received NMN saw increases in these levels and improvements to skeletal muscle metabolism. However, longer treatments may be needed to fully reverse aging effects and increase lifespan, as muscle strength was not improved after just one week of treatment. While promising, more research is needed to understand the genetic factors and potential human applications of NMN supplements.

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    51 views2 pages

    Nad Paper Needs Citations

    Uploaded by

    api-356726608
    This experiment tested the effects of nicotinamide mononucleotide (NMN), a precursor of NAD+, on mouse metabolism and aging. Mice who did not receive NMN showed declining levels of NAD+, ATP, and COX as they aged. Mice who received NMN saw increases in these levels and improvements to skeletal muscle metabolism. However, longer treatments may be needed to fully reverse aging effects and increase lifespan, as muscle strength was not improved after just one week of treatment. While promising, more research is needed to understand the genetic factors and potential human applications of NMN supplements.

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    This experiment examined the causes of loss of mitochondrial function with age.

    Specifically, the experiment tested the influence of the gene SIRT-1s expression on the
    metabolism of mice and the effects of Nicotinamide mononucleotide (NMN) - a precursor of
    NAD+. The goal of the experiment was to determine if the introduction of NMN would increase
    the mouses production of NAD+ and improve the metabolism of the mice that received it. Mice
    who were not given the NMN precursor were found to have declining levels of NAD+, ATP, and
    COX as they aged. SIRT-1 is a gene that produces a protein called sirtuin-1 and influences the
    regulation of NAD+ in the cell (it is regulated by the availability of intracellular NAD+). As the
    function of NAD+ is to transport electrons during cellular respiration (the generation of ATP
    from glucose), its presence is essential to the overall efficiency of the metabolism.
    When an organisms metabolism is efficient and coupled with caloric restriction to reduce
    the production of free radicals free electrons associated with molecular damage and increased
    mortality it appears to have the potential to increase the lifespan of said organism. During the
    experiment, after knocking out SIRT-1 the presence of COX and ATP decreased in the mice
    resulting in the metabolisms of the mice becoming less efficient (they resembled the metabolisms
    of older mice). This implies that the presence of SIRT-1 is essential to maintaining metabolic
    function. After receiving the NMN precursor, there was a marked increase in the NAD+, ATP,
    and COX levels in the mice. The study found that there was a correlation between the expression
    of the SIRT-1 gene and the metabolic efficiency of the tested mice.
    According to the study, the treatment of old mice with NMN reversed all of these
    biochemical aspects of aging and switched gastrocnemius muscle to a more oxidative fiber type
    (Gomes) showing that the supplement does positively impact the metabolism of the treated
    mices skeletal muscle. While the experiment did, in fact, show that the older mices declining
    metabolic function was reversed after being given the NMN precursor, the tissue that was tested
    in the mice was skeletal tissue, and is not the sole variable in the lifespan of mammals.
    Furthermore, the study concluded by stating 1 week of treatment might not be sufficient to
    reverse whole-organism aging and that longer treatments might be required since there was no
    observable improvement in muscle strength (Gomes). Therefore, it is not possible to
    conclusively state that the NMN supplement extended the mices lifespan significantly and did
    not merely create well-muscled elderly mice.
    I personally believe that the information gleaned from this experiment is valuable and
    should be studied further - particularly the genetic determinants of metabolism. There are
    certainly effective applications for this supplement, but the same can be said about blood doping.
    Since mice and humans have very similar genomes, the applications of this supplement should
    extend across species. The National Human Genome Research Institute states that of the 4,000
    genes that have been studied, less than 10 are found in one species but not the other (Why
    Mouse Matters). Assuming that researchers can find the equivalent SIRT-1 gene in humans, I
    dont see why the NMN precursor applied to humans wouldnt produce similar results to those of
    the mice that were tested in this experiment.
    Works Cited:
    Gomes, A., et al. (2014). Declining NAD+ Induces a Pseudohypoxic State Disrupting
    Nuclear-Mitochondrial Communication during Aging. Bethesda, National Institute of
    Health.
    (2000). Why Mouse Matters. Bethesda, National Human Genome Research Institute.

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