Evidence map›Paper›PMID 34899610›Full record

ArticleFrontiers in endocrinology2021

Genetic Correlation and Bidirectional Causal Association Between Type 2 Diabetes and Pulmonary Function.

Jiahao Zhu, Huanling Zhao, Dingwan Chen, Lap Ah Tse, Sanjay Kinra, Yingjun Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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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 3 institutions in 2 countries.

Jiahao ZhuDepartment of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, Hangzhou, China.
Huanling ZhaoDepartment of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, Hangzhou, China.
Dingwan ChenDepartment of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, Hangzhou, China.
Lap Ah TseJC School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR, China.
Sanjay KinraDepartment of Non-Communicable Disease Epidemiology, London School of Hygiene & Tropical Medicine, London, United Kingdom.
Yingjun LiDepartment of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, Hangzhou, China.
Hangzhou Medical College · CNChinese University of Hong Kong · CNLondon School of Hygiene & Tropical Medicine · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Observational studies have shown possible bidirectional association between type 2 diabetes (T2D) and pulmonary function, but the causality is not well defined. The purpose of this study is to investigate genetic correlation and causal relationship of T2D and glycemic traits with pulmonary function. Methods: By leveraging summary statistics from large-scale genome-wide association studies, linkage disequilibrium score regression was first implemented to quantify genetic correlations between T2D, glycemic traits, and several spirometry indices. Then both univariable and multivariable Mendelian randomization analyses along with multiple pleiotropy-robust methods were performed in two directions to assess the causal nature of these relationships. Results: Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) showed significant genetic correlations with T2D and fasting insulin levels and suggestive genetic correlations with fasting glucose and hemoglobin A1c. In Mendelian randomization analyses, genetically predicted higher FEV1 (OR = 0.77; 95% CI = 0.63, 0.94) and FVC (OR = 0.82; 95% CI = 0.68, 0.99) were significantly associated with lower risk of T2D. Conversely, genetic predisposition to higher risk of T2D exhibited strong association with reduced FEV1 (beta = -0.062; 95% CI = -0.100, -0.024) and FEV1 (beta = -0.088; 95% CI = -0.126, -0.050) and increased FEV1/FVC ratio (beta = 0.045; 95% CI = 0.012, 0.078). We also found a suggestive causal effect of fasting glucose on pulmonary function and of pulmonary function on fasting insulin and proinsulin. Conclusions: The present study provided supportive evidence for genetic correlation and bidirectional causal association between T2D and pulmonary function. Further studies are warranted to clarify possible mechanisms related to lung dysfunction and T2D, thus offering a new strategy for the management of the two comorbid diseases.

Indexed as

Blood GlucoseCausalityDiabetes Mellitus, Type 2FastingGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInsulinLinkage DisequilibriumLungLung DiseasesMendelian Randomization AnalysisMeta-Analysis as TopicPolymorphism, Single NucleotideRespiratory Function TestsBlood GlucoseInsulinglycemic traitslinkage disequilibrium score regressionMendelian randomizationpulmonary functiontype 2 diabetes

Identifiers

PMID34899610
PMCPMC8655865
OpenAlexW3217497072

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.