Evidence map›Paper›PMID 37305035›Full record

ArticleFrontiers in endocrinology2023

Causal relationship between circulating immune cells and the risk of type 2 diabetes: a Mendelian randomization study.

Jin Li, Qingmin Niu, Aiwei Wu, Yuchu Zhang, Liquan Hong, Hu Wang

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  13. Genetic support for the causal association between 91 circulating inflammatory proteins and atopic dermatitis: A two-sample Mendelian randomization trial.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 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

6 authors.

Jin LiKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.
Qingmin NiuKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.
Aiwei WuKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.
Yuchu ZhangKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.
Liquan HongKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.
Hu WangKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, The Third People's Hospital of Deqing, Deqing Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Though type 2 diabetes (T2D) has been known as a metabolic disease caused by multiple factors, the etiology remains insufficiently understood. Here, we aimed to figure out whether circulating immune cell profiles causally impact T2D liability. Methods: We applied one genome-wide association study (GWAS) summary statistics of blood traits in 563,085 participants from the Blood Cell Consortium and another GWAS of flow cytometric profile of lymphocyte subsets comprising 3,757 Sardinians to identify genetically predicted blood immune cells. We also obtained GWAS summary statistics in 898,130 individuals from the DIAGRAM Consortium to evaluate genetically predicted T2D. We primarily used inverse variance weighted (IVW) and weighted median methods to perform Mendelian randomization analyses and sensitivity analyses to evaluate heterogeneity and pleiotropy. Results: For circulating blood leukocyte and its subpopulations, the increase of genetically predicted circulating monocyte count was causally correlated with a higher risk of T2D [odds ratio (OR) = 1.06, 95% confidence interval (CI) = 1.02-1.10, p = 0.0048]. For lymphocyte subsets, CD8 Conclusions: These findings demonstrated that higher circulating monocyte and T-lymphocyte subpopulation predicted increased T2D susceptibility, which confirmed the immunity predisposition for T2D. Our results may have the potential to provide new therapeutic targets for the diagnosis and treatment of T2D.

Indexed as

Diabetes Mellitus, Type 2CD8-Positive T-LymphocytesGenome-Wide Association StudyHumansLeukocytesMendelian Randomization Analysiscirculating immune cellsgenome wide association study (GWAS)Mendelian randomization (MR)monocytetype 2 diabetes (T2D)

Identifiers

PMID37305035
PMCPMC10247959

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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.