Evidence map›Paper›PMID 36371056›Full record

ArticleJournal of advanced research2023

Sulforaphane-driven reprogramming of gut microbiome and metabolome ameliorates the progression of hyperuricemia.

Ruoyu Wang, Mairepaiti Halimulati, Xiaojie Huang, Yuxin Ma, Lutong Li, Zhaofeng Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
8.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 64 citations in OpenAlex.

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  11. From Mechanisms to Diseases: The Succinate-GPR91 Axis in Cardiometabolic Diseases.Journal of cardiovascular translational research · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ruoyu WangDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China.
Mairepaiti HalimulatiDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China.
Xiaojie HuangDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China.
Yuxin MaDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China.
Lutong LiDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China.
Zhaofeng ZhangDepartment of Nutrition and Food Hygiene, School of Public Health, Peking University, Haidian District, Beijing 100191, People's Republic of China; Beijing's Key Laboratory of Food Safety Toxicology Research and Evaluation, Beijing 100191, People's Republic of China. Electronic address: zhangzhaofeng@bjmu.edu.cn.
Peking University · CNChina National Center for Food Safety Risk Assessment · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCurrently, revealing how to prevent and control hyperuricemia has become an essential public health issue. Sulforaphane hasawiderangeofapplications in the management of hyperuricemia.

objectiveThe study objective was to verify the uric acid-lowering effects and the regulation of the gut-kidney axis mediated by sulforaphane and identify host-microbial co-metabolites in hyperuricemia.

methodsA hyperuricemia model was established by administering feedstuffs with 4% potassium oxonate and 20% yeast. Forty male Sprague-Dawley rats were randomly divided into the normal control, hyperuricemia, allopurinol, and sulforaphane groups. Animals were treated by oral gavage for six consecutive weeks, and then phenotypic parameters, metabolomic profiling, and metagenomicsequencing were performed.

resultsSulforaphane could lower uric acid by decreasing urate synthesis and increasing renal urate excretion in hyperuricemic rats (P<0.05). We identified succinic acid and oxoglutaric acid as critical host-gut microbiome co-metabolites. Moreover, sulforaphane improved the diversity of microbial ecosystems and functions, as well as metabolic control of the kidney. Notably, sulforaphane exerted its renoprotective effect through epigenetic modification of Nrf2 and interaction between gut microbiota and epigenetic modification in hyperuricemic rats.

conclusionWe revealed that sulforaphane could ameliorate the progression of hyperuricemia by reprogramming the gut microbiome and metabolome. Our findings may provide a good means for efficiently preventing and treating hyperuricemia.

Indexed as

Gastrointestinal MicrobiomeHyperuricemiaAnimalsEcosystemIsothiocyanatesMaleMetabolomeRatsRats, Sprague-DawleySulfoxidesUric AcidIsothiocyanatessulforaphaneSulfoxidesUric AcidGut microbiotaHost-gut microbiome co-metaboliteHyperuricemiaSulforaphane

Identifiers

PMID36371056
PMCPMC10555773
OpenAlexW4308891224

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.