Evidence map›Paper›PMID 36289225›Full record

ArticleNature communications2022

Functional and metabolic alterations of gut microbiota in children with new-onset type 1 diabetes.

Xiaoxiao Yuan, Ruirui Wang, Bing Han, ChengJun Sun, Ruimin Chen, Haiyan Wei, Linqi Chen, Hongwei Du, Guimei Li, Yu Yang and 17 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 3 pooled it
11.3field-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

107 citing papers in PubMed, 3 syntheses or guidelines pooled it, 140 citations in OpenAlex.

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47 more citing papers are in PubMed but not listed here.

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

27 authors at 15 institutions in 1 country.

Xiaoxiao Yuan *Department of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.ORCID 0000-0003-2405-0101
Ruirui Wang *Shanghai Innovation Center of TCM Health Service, Shanghai University of Traditional Chinese Medicine, Shanghai, China.ORCID 0000-0002-2766-9420
Bing HanInstitute of Pediatrics, Children's Hospital of Fudan University, Shanghai, China.
ChengJun SunDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.ORCID 0000-0001-6025-4801
Ruimin ChenFuzhou Children's Hospital of Fujian Medical University, Fuzhou, China.
Haiyan WeiDepartment of Endocrinology and Inherited Metabolic, Children's Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Linqi ChenChildren's Hospital of Soochow University, Suzhou, China.
Hongwei DuThe First Hospital of Jilin University, Changchun, China.
Guimei LiDepartment of Pediatric Endocrinology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Yu YangThe Affiliated Children's Hospital of Nanchang University, Nanchang, China.
Xiaojuan ChenDepartment of Endocrinology, Genetics and Metabolism, The Children's Hospital of Shanxi Province, Taiyuan, China.
Lanwei CuiThe First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhenran XuDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.ORCID 0000-0003-2718-6717
Junfen FuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6405-1251
Jin WuDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Wei GuDepartment of Endocrinology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Zhihong ChenDepartment of Neuroendocrinology Pediatrics, Affiliated Hospital of Qingdao University, Qingdao, China.
Xin FangFujian Medical University Union Hospital, Fuzhou, China.ORCID 0000-0002-3323-8221
Hongxiu YangQingdao Women and Children's Hospital, Qingdao, China.
Zhe SuShenzhen Children's Hospital, Shenzhen, China.
Jing WuDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.
Qiuyue LiDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.ORCID 0000-0003-1825-5231
Miaoying ZhangDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China.ORCID 0000-0002-4160-3962
Yufeng ZhouInstitute of Pediatrics, Children's Hospital of Fudan University, and the Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.ORCID 0000-0002-6050-4951
Lei ZhangShanghai Innovation Center of TCM Health Service, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Guang JiInstitute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. jg@shutcm.edu.cn.ORCID 0000-0003-0842-3676
Feihong LuoDepartment of Pediatric Endocrinology and Inherited Metabolic Diseases, Children's Hospital of Fudan University, Shanghai, China. luofh@fudan.edu.cn.
Children's Hospital of Fudan University · CNShanghai University of Traditional Chinese Medicine · CNFudan University · CNFujian Medical University · CNQingdao University · CNSichuan University · CNChildren's Hospital of Zhejiang University · CNHarbin Medical University · CNJilin University · CNNanchang University · CNSecond Affiliated Hospital of Nanjing Medical University · CNShandong Provincial Hospital · CNShenzhen Children's Hospital · CNSoochow University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gut dysbiosis has been linked to type 1 diabetes (T1D); however, microbial capacity in T1D remains unclear. Here, we integratively profiled gut microbial functional and metabolic alterations in children with new-onset T1D in independent cohorts and investigated the underlying mechanisms. In T1D, the microbiota was characterized by decreased butyrate production and bile acid metabolism and increased lipopolysaccharide biosynthesis at the species, gene, and metabolite levels. The combination of 18 bacterial species and fecal metabolites provided excellently discriminatory power for T1D. Gut microbiota from children with T1D induced elevated fasting glucose levels and declined insulin sensitivity in antibiotic-treated mice. In streptozotocin-induced T1D mice, butyrate and lipopolysaccharide exerted protective and destructive effects on islet structure and function, respectively. Lipopolysaccharide aggravated the pancreatic inflammatory response, while butyrate activated Insulin1 and Insulin2 gene expression. Our study revealed perturbed microbial functional and metabolic traits in T1D, providing potential avenues for microbiome-based prevention and intervention for T1D.

Indexed as

Diabetes Mellitus, Type 1Gastrointestinal MicrobiomeAnimalsAnti-Bacterial AgentsBile Acids and SaltsButyratesGlucoseLipopolysaccharidesMiceStreptozocinAnti-Bacterial AgentsBile Acids and SaltsButyratesGlucoseLipopolysaccharidesStreptozocin

Identifiers

PMID36289225
PMCPMC9606127
OpenAlexW4307291327

What OpenQuestion holds

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LicenceCC BY
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.