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    Home > Active Ingredient News > Immunology News > Li Xiangkai’s team from Lanzhou University found that Lactobacillus in Northwest Gourmet syrup may lower uric acid

    Li Xiangkai’s team from Lanzhou University found that Lactobacillus in Northwest Gourmet syrup may lower uric acid

    • Last Update: 2021-04-14
    • Source: Internet
    • Author: User
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    iNature's purine-rich foods are not completely degraded into uric acid (UA) in the human body, resulting in a high content of UA in plasma, which is considered to be an important risk factor for diseases such as gout.

    Recent studies on the beneficial effects of fermented foods show that such foods can effectively control hyperuricemia and gout.

    On March 25, 2021, the Li Xiangkai team of Lanzhou University published an online research paper entitled "Limosilactobacillus fermentum JL-3 isolated from "Jiangshui" ameliorates hyperuricemia by degrading uric acid" in Gut Microbes (IF=7.
    74), a well-known journal in the field of microbiology.
    Studies have isolated Lactobacillus fermentum JL-3 from the traditional fermented food slurry in Northwest China, and found that the slurry can control the accumulation of uric acid by degrading uric acid in animals.

    After 15 days of oral administration to mice, JL-3 colonization was continuously detected in the feces of the mice.

    The level of UA in the urine of mice fed with JL-3 was similar to that of control mice.

    The serum UA level of the former was significantly lower than that of the control group (31.
    3%), further confirming the UA reduction effect of the JL-3 strain.

    The JL-3 strain also restored some inflammatory markers and oxidative stress indicators related to hyperuricemia (IL-1β, MDA, CRE, blood urea nitrogen), and the intestinal microbial diversity results showed that JL-3 can Regulate the release of intestinal microbiota.

    Therefore, Lactobacillus fermentum JL-3 strain can effectively reduce the UA level of mice and can be used as an auxiliary therapeutic agent for the treatment of hyperuricemia.

    Hyperuricemia is one of the main metabolic diseases related to gout, and it is on the rise in many countries.

    Some studies report that the prevalence of gout is 1% to 3% in Europe and 3.
    9% in the United States.

    In addition, there were an estimated 7.
    44 million gout cases worldwide in 2017.

    According to the "Gout Report White Paper" (2017), the number of hyperuricemia patients in China has reached 170 million, an annual growth rate of 9.
    7%.

    Foods rich in purines are not completely degraded into UA in the human body, resulting in high levels of UA in plasma, which is considered to be an important risk factor for diseases such as gout.

    High levels of UA in plasma have long been associated with hyperuricemia.

    There are two ways to accumulate UA in humans.

    The first is the endogenous accumulation caused by the lack of enzymes in the purine metabolism pathway; the other way of UA accumulation is through ingestion and exogenous absorption of purine-rich foods.

    A recent study showed that eating meat will increase the risk of gout by 21%, while eating seafood will only increase the risk by 7%.

    External intervention can effectively alleviate hyperuricemia.

    However, purines can greatly affect the effectiveness of the intestinal flora.

    Currently, there are several methods for hyperuricemia, including diet, drugs, and biological therapies, which aim to treat hyperuricemia through the uptake and degradation of purines.

    For example, allopurinol, a representative drug that lowers UA, can competitively bind with xanthine oxidase (XOD) to reduce the production of UA.

    Febuxostat is another novel non-purine XOD selective inhibitor.

    Both drugs are widely used to treat hyperuricemia and are relatively safe.

    Dietary interventions work by limiting the intake of high-purine foods.

    As a cost-effective treatment method, microbial repair has minimal damage to parts of the body, so it has been widely accepted by the public.

    Therefore, several strains of Lactobacillus that can utilize purines have been discovered.

    Among these strains, it was found to be effective in reducing rodent UA levels.

    For example, Lactobacillus brevis (DM9218) and Lactobacillus gasseri (PA-3) degrade the intermediate products of purine metabolism to improve hyperuricemia.

    Fermented food is rich in lactic acid bacteria, which can produce organic acids to control rotting microorganisms and pathogens.

    Studies have shown that fermented foods such as yogurt are beneficial to patients with type 2 diabetes due to their rich content of lactic acid bacteria.

    According to reports, there are 30 kinds of probiotics that can effectively degrade UA.

    "Jingshui" is a traditional fermented food in northwestern China.
    It is made from vegetables, such as celery and cabbage.

    Lactic acid bacteria, acetic acid bacteria and yeasts are the main microorganisms in the process of slurry fermentation.

    The study isolated Lactobacillus fermentum JL-3 from the traditional fermented food slurry in Northwest China, and found that the slurry can control the accumulation of uric acid by degrading uric acid in animals.

    After 15 days of oral administration to mice, JL-3 colonization was continuously detected in the feces of the mice.

    The level of UA in the urine of mice fed with JL-3 was similar to that of control mice.

    The serum UA level of the former was significantly lower than that of the control group (31.
    3%), further confirming the UA reduction effect of the JL-3 strain.

    The JL-3 strain also restored some inflammatory markers and oxidative stress indicators related to hyperuricemia (IL-1β, MDA, CRE, blood urea nitrogen), and the intestinal microbial diversity results showed that JL-3 can Regulate the release of intestinal microbiota.

    Therefore, Lactobacillus fermentum JL-3 strain can effectively reduce the UA level of mice and can be used as an auxiliary therapeutic agent for the treatment of hyperuricemia.

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