<i>Lactobacillus fermentum</i>F40-4 ameliorates hyperuricemia by modulating the gut microbiota and alleviating inflammation in mice

Cao, Jiayuan; Wang, Ting; Liu, Yisuo; Zhou, Wei; Hao, Haining; Liu, Qiqi; Yin, Boxing; Yi, Huaxi

doi:10.1039/d2fo03701g

Cited by 8 publications

(4 citation statements)

References 46 publications

(74 reference statements)

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“…Similar studies have shown that Lacticaseibacillus rhamnosus 1155 and Limosilactobacillus fermentum 2644 can effectively reduce the levels of inflammation and oxidative damage in rats with hyperuricemia [48]. It was discovered that Lactobacillus fermentum F40-4 alleviated the level of liver and kidney damage in hyperuricemia [49]. These results suggest that ASC-1 can relieve the inflammation and oxidative stress induced by hyperuricemia.…”

Section: Asc-1 Alleviated Inflammation and Oxidative Stress In Hyperu...mentioning

confidence: 53%

Priestia megaterium ASC-1 Isolated from Pickled Cabbage Ameliorates Hyperuricemia by Degrading Uric Acid in Rats

Zhu,

Bi,

Fang

et al. 2024

Microorganisms

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Pickled cabbage, a traditional fermented food rich in functional microorganisms, can effectively control hyperuricemia and gout. In this study, a Priestia megaterium ASC-1 strain with strong uric acid (UA) degradation ability was isolated from pickled cabbage. After oral administration for 15 days, ASC-1 was stably colonized in the rats in this study. ASC-1 significantly reduced UA levels (67.24%) in hyperuricemic rats. Additionally, ASC-1 alleviated hyperuricemia-related inflammatory response, oxidative stress, and blood urea nitrogen. Intestinal microbial diversity results showed that ASC-1 restored intestinal injury and gut flora dysbiosis caused by hyperuricemia. These findings suggest that P. megaterium ASC-1 may be used as a therapeutic adjuvant for the treatment of hyperuricemia.

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Section: Asc-1 Alleviated Inflammation and Oxidative Stress In Hyperu...mentioning

confidence: 53%

Priestia megaterium ASC-1 Isolated from Pickled Cabbage Ameliorates Hyperuricemia by Degrading Uric Acid in Rats

Zhu,

Bi,

Fang

et al. 2024

Microorganisms

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“…[31,32] Flavonoids, folate, probiotics, anthocyanins, fibers and other anti-inflammatory dietary components have been shown to reduce blood uric acid levels and improve hyperuricemia through mechanisms such as downregulating inflammatory pathways and modulating intestinal homeostasis. [15,16,[33][34][35][36][37] Further research is needed to elucidate the relationship between the inflammatory potential of food and hyperuricemia.…”

Section: Discussionmentioning

confidence: 99%

Association of dietary inflammatory index with all-cause and cardiovascular disease mortality in hyperuricemia population: A cohort study from NHANES 2001 to 2010

Huang,

Zhang,

et al. 2023

Medicine

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Dietary management is a crucial component of non-pharmacological treatment for hyperuricemia, yet there is a paucity of research on the impact of dietary habits on the survival outcomes of individuals with hyperuricemia. The objective of this study is to examine the association between dietary inflammatory index (DII) and the all-cause and cardiovascular disease (CVD) mortality in individuals with hyperuricemia. This study included 3093 adult participants from National Health and Nutrition Examination Survey (NHANES) 2001 to 2010. Participants were categorized into 4 groups based on quartiles of DII to demonstrate data characteristics, with sample weights considered. The relationship between DII and the risk of hyperuricemia was examined using multivariable logistic regression models. Kaplan–Meier models and Cox proportional hazards models were employed to assess the relationship between DII levels and the all-cause mortality in individuals with hyperuricemia, with the non-linear relationship tested using restricted cubic splines (RCS). Competing risk models were employed to investigate the association between DII levels and the CVD mortality in individuals diagnosed with hyperuricemia. Subgroup and sensitivity analysis were performed to confirm the robustness and reliability of the findings. Among the participants, 47.95% were aged over 60 years. A positive association observed between the highest quartile of DII level and the incidence of hyperuricemia (OR: 1.34, CI [1.13, 1.57]). Elevated DII levels were correlated with increased all-cause mortality (P value < .001) and CVD mortality (P value < .001) in participants. In comparison to the lowest quartile, the highest quartile of DII exhibited a 31% rise in all-cause mortality (HR: 1.31, CI [1.01, 1.68]) and a 50% increase in CVD mortality (HR: 1.50, CI [1.00, 2.26]). No indication of a nonlinear association between DII levels and all-cause mortality (p-non-linear = .43). These findings indicate a positive correlation between the pro-inflammatory diet and the incidence of hyperuricemia. Additionally, a pro-inflammatory diet may elevate the all-cause and CVD mortality in individuals with hyperuricemia.

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“…XOD inhibitors or uricases, which catalyse uric acid into a more soluble product, can prevent hyperuricemia. Cao et al [56] found in mice experiments that L. fermentum F40-4 can reduce the level of XOD and improve uric acid levels by inhibiting inflammatory responses and reshaping the gut microbiota. UA419 significantly reduced serum markers, including uric acid, XOD and inflammatory cytokines.…”

Section: New Proposals For Gout Therapy Probioticsmentioning

confidence: 99%

Gut microbiota plays a significant role in gout

Feng,

Wang,

Xin

et al. 2024

Journal of Medical Microbiology

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With the development of social economy, the incidence of gout is increasing, which is closely related to people’s increasingly rich diet. Eating a diet high in purine, fat, sugar and low-fibre for a long time further aggravates gout by affecting uric acid metabolism. The renal metabolism mechanism of uric acid has been thoroughly studied. To find a new treatment method for gout, increasing studies have recently been conducted on the mechanism of intestinal excretion, metabolism and absorption of uric acid. The most important research is the relationship between intestinal microbiota and the risk of gout. Gut microbiota represent bacteria that reside in a host’s gastrointestinal tract. The composition of the gut microbiota is associated with protection against pathogen colonization and disease occurrence. This review focuses on how gut microbiota affects gout through uric acid and discusses the types of bacteria that may be involved in the occurrence and progression of gout. We also describe potential therapy for gout by restoring gut microbiota homeostasis and reducing uric acid levels. We hold the perspective that changing intestinal microbiota may become a vital method for effectively preventing or treating gout.

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Lactobacillus fermentumF40-4 ameliorates hyperuricemia by modulating the gut microbiota and alleviating inflammation in mice

Abstract: Hyperuricemia (HUA) is a systemic disease characterized by the disorder of purine metabolism and the abnormal increase of serum uric acid (UA). Probiotics can exert potential therapeutic benefits to some...

Cited by 8 publications

References 46 publications

Priestia megaterium ASC-1 Isolated from Pickled Cabbage Ameliorates Hyperuricemia by Degrading Uric Acid in Rats

Priestia megaterium ASC-1 Isolated from Pickled Cabbage Ameliorates Hyperuricemia by Degrading Uric Acid in Rats

Association of dietary inflammatory index with all-cause and cardiovascular disease mortality in hyperuricemia population: A cohort study from NHANES 2001 to 2010

Gut microbiota plays a significant role in gout

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