Evidence map›Paper›PMID 32298241›Full record

ArticleJCI insight2020

Gut microbial metabolites alter IgA immunity in type 1 diabetes.

Juan Huang, James A Pearson, Jian Peng, Youjia Hu, Sha Sha, Yanpeng Xing, Gan Huang, Xia Li, Fang Hu, Zhiguo Xie and 6 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 84 citations in OpenAlex.

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  17. Role of short-chain fatty acids in host physiology.Animal models and experimental medicine · 2024
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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

16 authors at 3 institutions in 3 countries.

Juan HuangDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
James A PearsonSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Jian PengSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Youjia HuSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Sha ShaSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Yanpeng XingSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Gan HuangDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Xia LiDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Fang HuDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Zhiguo XieDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Yang XiaoDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Shuoming LuoDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Chen ChaoDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
F Susan WongDivision of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Zhiguang ZhouDepartment of Metabolism and Endocrinology, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan, China.
Li WenSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Central South University · CNYale University · USCardiff University · GB

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold, GERALD I SHULMAN · 1993 to 2026
$44.0M
Investigating the early development of the immune system and islet autoimmunity later in lifeR01HD097808 · NICHD · YALE UNIVERSITY · PI WEN, LI · 2019 to 2021
$1.3M
NCATS NIH HHS UL1 TR001863NICHD NIH HHS R01 HD097808NIDDK NIH HHS P30 DK045735
6 · The paper itself

Abstract

The incidence of type 1 diabetes (T1D) has been increasing among children and adolescents, in which environmental factors, including gut microbiota, play an important role. However, the underlying mechanisms are yet to be determined. Here, we show that patients with newly diagnosed T1D displayed not only a distinct profile of gut microbiota associated with decreased short-chain fatty acids (SCFAs) production, but also an altered IgA-mediated immunity compared with healthy control subjects. Using germ-free NOD mice, we demonstrate that gut microbiota from patients with T1D promoted different IgA-mediated immune responses compared with healthy control gut microbiota. Treatment with the SCFA, acetate, reduced gut bacteria-induced IgA response accompanied by decreased severity of insulitis in NOD mice. We believe our study provides new insights into the functional effects of gut microbiota on inducing IgA immune response in T1D, suggesting that SCFAs might be potential therapeutic agents in T1D prevention and/or treatment.

Indexed as

Diabetes Mellitus, Type 1AdolescentAnimalsChildFatty Acids, VolatileFemaleGastrointestinal MicrobiomeHumansImmunoglobulin AMaleMiceMice, Inbred NODFatty Acids, VolatileImmunoglobulin AAutoimmunityDiabetesTranslation

Identifiers

PMID32298241
PMCPMC7259536
OpenAlexW3017053315

What OpenQuestion 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 OpenQuestion graph.