Evidence map›Paper›PMID 35246764›Full record

ArticleEndocrine2022

Changes of gut microbiota in diabetic nephropathy and its effect on the progression of kidney injury.

Kedan Cai, Yanhong Ma, Fanghao Cai, Xiaohan Huang, Liang Xiao, Chenyu Zhong, Pingping Ren, Qun Luo, Jianghua Chen, Fei Han

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
8.6field-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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Kedan Cai *HwaMei Hospital, University of Chinese Academy of Sciences; Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, China.
Yanhong Ma *Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Fanghao CaiKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Xiaohan HuangKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Liang XiaoKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Chenyu ZhongHwaMei Hospital, University of Chinese Academy of Sciences; Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, China.
Pingping RenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Qun LuoHwaMei Hospital, University of Chinese Academy of Sciences; Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, China.
Jianghua ChenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China.
Fei HanKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, China. hanf8876@zju.edu.cn.ORCID 0000-0001-5363-7556
Zhejiang Center for Disease Control and Prevention · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe aimed to illustrate gut microbiota and short chain fatty acid (SCFA) levels in diabetic nephropathy (DN) patients, and investigate the mechanism of sodium butyrate in diabetic mellitus (DM) rats.

methodsGut microbiota and serum SCFA levels were measured by 16S rDNA and GC-MS. After being built by streptozotocin (DM rats), the DM rats were administered 300 mg/kg sodium butyrate for 12 weeks (DM + BU rats). Gut microbiota, serum and fecal butyrate level were measured. RT-PCR, WB and transmission electron microscopy were performed to explore LC3mRNA or LC3B protein expression, and autophagosomes in kidney tissues. AMPK/mTOR protein expression in renal tissue were also measured.

resultsThe gut microbial dysbiosis was found in DM and DN groups, and some SCFAs-producing bacteria were decreased in DN group. The serum butyrate concentrations were lower in SCFA-DN group compared with SCFA-HC group and SCFA-DM group in the other cohort. Serum butyrate level was positively correlated with eGFR. Sodium butyrate increased serum and fecal butyrate levels, and improved the enlargement of glomerular area and fibronectin and collagen IV expressions in renal tissues in DM + BU rats. The LC3 mRNA, LC3BII/I ratio and number of autophagosomes were increased in renal tissue of DM + BU rats. Higher p-AMPK/AMPK ratio and lower p-mTOR/ mTOR ratio were shown in renal tissue of DM + BU rats compared with DM rats.

conclusionsWe found the decrease in SCFAs-producing bacteria and low SCFAs concentrations in DN patients. Oral butyrate supplementation may improve kidney injury in DM rats, possibly by increasing autophagy via activating AMPK/mTOR pathway.

Indexed as

Diabetes MellitusDiabetic NephropathiesGastrointestinal MicrobiomeAMP-Activated Protein KinasesAnimalsButyric AcidFatty Acids, VolatileFemaleHumansKidneyMaleRatsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesButyric AcidFatty Acids, VolatileTOR Serine-Threonine KinasesAutophagyButyrateDiabetic nephropathyGut microbiomeShort chain fatty acid

Identifiers

PMID35246764
OpenAlexW4220948202

What Socratic holds

Textmetadata
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 Socratic graph.