Evidence map›Paper›PMID 36800530›Full record

ArticleDiabetes care2023

Gastrointestinal Consequences of Type 2 Diabetes Mellitus and Impaired Glycemic Homeostasis: A Mendelian Randomization Study.

Jie Chen, Shuai Yuan, Tian Fu, Xixian Ruan, Jie Qiao, Xiaoyan Wang, Xue Li, Dipender Gill, Stephen Burgess, Edward L Giovannucci and 1 more

Abstract read
In one paragraph

Article in Diabetes care, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 7 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

61 citing papers in PubMed, 7 syntheses or guidelines pooled it.

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

4 · The record

Corrections and comments

  • Commented on by
    2023
5 · Who and what money

Authors and funding

11 authors.

Jie ChenSchool of Public Health and The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.ORCID 0000-0002-4029-4192
Shuai YuanUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Tian FuDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xixian RuanDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Jie QiaoDepartment of Endocrinology and Metabolism, the Second Affiliated Hospital of ZheJiang University School of Medicine, Hangzhou, China.
Xiaoyan WangDepartment of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, China.
Xue LiSchool of Public Health and The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Dipender GillDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, U.K.
Stephen BurgessMRC Biostatistics Unit, University of Cambridge, Cambridge, U.K.
Edward L GiovannucciDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA.
Susanna C LarssonUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Funding

British Heart Foundation RE/18/4/34215Medical Research Council MC_UU_00002/7Wellcome TrustWellcome Trust 203928/Z/16/Z
6 · The paper itself

Abstract

objectiveWe conducted a Mendelian randomization (MR) study to examine the associations of type 2 diabetes and glycemic traits with gastrointestinal diseases (GDs). RESEARCH DESIGN AND

methodsUncorrelated genetic variants associated with type 2 diabetes (n = 231), fasting insulin (n = 38), fasting glucose (n = 71), and hemoglobin A1c (n = 75) at the genome-wide significance were selected as instrument variables. Genetic associations with 23 common GDs were obtained from the FinnGen and UK Biobank studies and other large consortia.

resultsGenetic liability to type 2 diabetes was associated with the risk of 12 GDs. Per 1-unit increase in the log-transformed odds ratio (OR) of type 2 diabetes, the OR was 1.06 (95% CI, 1.03-1.09) for gastroesophageal reflux disease, 1.12 (95% CI, 1.07-1.17) for gastric ulcer, 1.11 (95% CI, 1.03-1.20) for acute gastritis, 1.07 (95% CI, 1.01-1.13) for chronic gastritis, 1.08 (95% CI, 1.03-1.12) for irritable bowel syndrome, 1.04 (95% CI, 1.01-1.07) for diverticular disease, 1.08 (95% CI, 1.02-1.14) for acute pancreatitis, 1.09 (95% CI, 1.05-1.12) for cholelithiasis, 1.09 (95% CI, 1.05-1.13) for cholelithiasis with cholecystitis, 1.29 (95% CI, 1.17-1.43) for nonalcoholic fatty liver disease, 1.12 (95% CI, 1.03-1.21) for liver cirrhosis, and 0.93 (95% CI, 0.89-0.97) for ulcerative colitis. Genetically predicted higher levels of fasting insulin and glucose were associated with six and one GDs, respectively.

conclusionsAssociations were found between genetic liability to type 2 diabetes and an increased risk of a broad range of GDs, highlighting the importance of GD prevention in patients with type 2 diabetes.

Indexed as

CholelithiasisDiabetes Mellitus, Type 2GastritisPancreatitisAcute DiseaseBlood GlucoseGenome-Wide Association StudyGlucoseHumansInsulinInsulin, Regular, HumanMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsBlood GlucoseGlucoseInsulinInsulin, Regular, Human

Identifiers

PMID36800530
PMCPMC10091506

What OpenQuestion holds

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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.