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    Home > Biochemistry News > Biotechnology News > Chinese scientists have opened the door between gut microbes and longevity.

    Chinese scientists have opened the door between gut microbes and longevity.

    • Last Update: 2020-08-25
    • Source: Internet
    • Author: User
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    Professor Wang Meng, a Chinese scientist from Baylor College of Medicine, led the team to screen for nearly 4,000 strains of E. coli with different mutations in the body, and found dozens of genes that can prolong life, delay tumor development, and build up beta-amyloid proteins. And found a compound that can "continue to live" - diaphragm isoic acid (colanic acid, CA)! In recent years, more and more studies have proved that changes in gut microorganisms are related to the aging process of the host, however, most of the research is limited to group studies and macrogenomic analysis, and the exploration of the genetic function and molecular mechanism of a single microorganism is still lacking.
    in this context, the significance of this study is undoubtedly very significant.
    It connects gut microbial-gene-aging-age-related diseases in series, and identifies specific compounds that play a role, providing new ideas for practical application of the study, which can be said to "open the door for gut microbes to resist aging and extend their life."
    not only, but at the same time as the discovery of CA, they also revealed that CA is using mitochondria to slow down aging.
    as an "energy factory" in cells, the relationship between mitochondria and aging has been found.
    but this study is the first to show that gut microbes can still "communicate" with mitochondria through metabolites.
    it seems that gut microbes can not only communicate with the far end of the organ, even the organ can, can really be considered "no holes in"! Why is E. coli the bias used in the study? Because the beautiful cryptobacteria eat bacteria such as E. coli, in the laboratory culture, usually in the culture of E. coli colonies, and then let the larvae of the worm live in it.
    E. coli will then proliferate in the intestines of the larvae, forming the intestinal microbiome of ne worms as they grow older.
    in this study, to gain a comprehensive and in-depth understanding of the effects of the E. coli gene level on longevity, the researchers created an E. coli single gene knockout bank that included 3,983 single-gene mutant strains.
    They fed each strain individually to the caterpillars, observed their life span, and after testing, the researchers found that 29 mutant bacteria can extend the life of the worm by more than 10%, the most significant of which is the hns mutation, this group of worm life extended by as much as 40%! In addition, the researchers tried to introduce the mutation into wild E. coli (MG1655) and found that 23 of them were still effective.
    , 21 bacteria maintain their ability to live longer, even after passing through the larvae and feeding mutants from the worm.
    this leads researchers to the idea that gut microbes have no doubt about the regulatory role of host life, and that these regulations are not related to the specific microbial strains and the stage of development of the host.
    means that any microorganism that has these mutations, no matter what stage of development they occur, can play a role in prolonging life.
    of course, if researchers want to "make" probiotics through genetic engineering to help us extend our lives, it seems feasible on the basis of this study! The "secret of longevity village" is no longer a secret.
    imagine, in the future, if we can drink a probiotic yogurt or something to extend the life, wouldn't it be the United States? Of course, living longer is not the ultimate goal, healthy living longer is the only thing.
    longevity is not really interesting if the disease is entangled, so the researchers also tested whether the mutant bacteria can cope with the disease caused by aging.
    Researchers asked the worms to express tumors caused by the proliferation of human beta-amyloid proteins and reproductive cells, and found 16 mutations that increased the survival of tumor
    , 14 mutations that prolonged the life of the "dementia" worm, and 12 mutations that delayed the "dementia" coybus from losing its ability to move.
    a total of 13 of these mutations appear, which play a "protective role" in both types of ventilants, which in a sense suggests that these 13 mutations can help improve the "quality of life" of the host as a whole.
    if we open a brain hole, maybe the probiotic yogurt we conceived earlier might also help some sick older people? In many years of research, scientists have revealed several molecular or signaling path mechanisms associated with longevity, including insulin/insulin-like growth factor 1 (IGF-1), repamycin target protein (TOR) signaling paths, and calorie restriction (caloric restriction, CR).
    the study, the researchers also found that most mutant bacteria extended the life of the worm through IGF-1 and TOR signaling paths, and that only four mutant bacteria passed calorie restriction.
    however, these results do not include two mutant bacteria, one is the hns mutation that maximizes the life of the worm, and the other is the lon mutation, which extends the life of the worm by 25%.
    These two mutations do not work through these three known pathways, which makes researchers wonder if the discovery of this "mystery pathway" means that we can get another effective hint in the "pass-through cheat" of longevity. As the researchers struggled, they suddenly found an "unusual" link between the two genes -- they were involved in the synthesis of a metabolite! This metabolite is diaphragm is polysaccharide (colanic acid, CA).
    then the researchers ventured to wonder if they were using CA as a molecule to extend the life of the worm. With bold guesses, they first tested the CA content in the medium and found that it was very high, and that the hns and lon mediums were higher than the others.
    In addition to prolonging life, these mutant bacteria containing large amounts of CA also weaken the breakdown of the muscle mitochondria associated with aging of the ventilants, the body wall muscle mitochondria decomposition, decreased function is a significant sign of soward cell aging.
    to prove CA's efficacy, the researchers fed CA directly to the caterpillars and found that they lived 20% longer! For worms with beta-amyloid proteins and germ cell tumors, CA intake also improves their motor ability and survival time.
    , fruit flies that ingested CA in experiments also showed an increase in life expectancy.
    so how does CA extend its life? This has to do with the mitochondria we just mentioned.
    after ingesting CA, it regulates the division of mitochondria and promotes the mitochondrial unfolded protein response.
    mitochondria are a very important kind of cellular device in all ethylithyritic cells, and are the "energy factory" of cells that supply energy to cells and participate in the regulation of cell growth.
    's findings seem to tell us that gut microbes "fuel" mitochondria with their metabolites, maintaining the "normal functioning" of energy plants so that mitochondria can tirelessly provide energy for cell activity and keep cells "young."
    decline or disorder in mitochondrial function is a sign and driver of aging, and protein non-folding is one of the causes of mitochondrial dysfunction.
    CA as a metabolite is absorbed by intestinal cells, and the mitochondria in the cell "establish a link" to help the stress conditions of the unfolded protein response, the correct folding, restore the signal conduction of mitochondria, maintain the function of mitochondria and protein stability, for the vendria "life-sustaining".
    addition, this mechanism can also occur in mammalian cells, and with the fruit flies in front of them, the researchers believe that the mechanism is evolutionaryly conservative.
    if you continue to dig deeper, the ca can help the unfolded protein response is through the transcription factor ATFS-1, such as the transgene of the atfs-1 gene mutation, so that ATFS-1 lost function, then CA extended life can not be achieved.
    , Professor Wang Meng said: "Mitochondria seem to have evolved from bacteria that entered cells millions of years ago.
    Our research shows that millions of years later, bacteria can still 'communicate' with mitochondria in our cells, which we think is important, and here we are providing the first evidence of communication between microbes and mitochondria.
    the Journal of Cells today, researchers from the National University of Singapore have written a commentary on the issue.
    They point out that two of the findings in this series are noteworthy, one is that CA helps with the response of unfolded proteins under stress conditions, suggesting that ca may be a way to counteract gut microbial stress in the future, which may be beneficial for many stress-producing diseases.
    is that the direct addition of molecules represented by CA is also an inspiration to humans.
    this goes back to what we called probiotic yogurt, and adding CA directly without probiotics seems like a good choice.
    Over all, this study, although conducted only in online worms, is critical to helping researchers better understand the relationship between gut microbes and aging, and the identification of key molecular compounds must have inspired us to see the hope of "longevity".
    .
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