Evidence map›Paper›PMID 32366963›Full record

ArticleScientific reports2020

Integrative analysis of Mendelian randomization and Bayesian colocalization highlights four genes with putative BMI-mediated causal pathways to diabetes.

Qian Liu, Jianxin Pan, Carlo Berzuini, Martin K Rutter, Hui Guo

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–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

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3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
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  7. Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023
    Review
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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

5 authors.

Qian LiuCentre for Biostatistics, School of Health Sciences, The University of Manchester, Manchester, UK.
Jianxin PanSchool of Mathematics, Faculty of Engineering and Physical Science, The University of Manchester, Manchester, UK.
Carlo BerzuiniCentre for Biostatistics, School of Health Sciences, The University of Manchester, Manchester, UK.ORCID http://orcid.org/0000-0001-6056-0489
Martin K RutterDivision of Endocrinology, Diabetes and Gastroenterology, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
Hui GuoCentre for Biostatistics, School of Health Sciences, The University of Manchester, Manchester, UK. hui.guo@manchester.ac.uk.ORCID http://orcid.org/0000-0003-0282-6933

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies have identified hundreds of single nucleotide polymorphisms (SNPs) that are associated with BMI and diabetes. However, lack of adequate data has for long time prevented investigations on the pathogenesis of diabetes where BMI was a mediator of the genetic causal effects on this disease. Of our particular interest is the underlying causal mechanisms of diabetes. We leveraged the summary statistics reported in two studies: UK Biobank (N = 336,473) and Genetic Investigation of ANthropometric Traits (GIANT, N = 339,224) to investigate BMI-mediated genetic causal pathways to diabetes. We first estimated the causal effect of BMI on diabetes by using four Mendelian randomization methods, where a total of 76 independent BMI-associated SNPs (R

Indexed as

Body Mass IndexGenetic Predisposition to DiseasePolymorphism, Single NucleotideDiabetes MellitusFemaleGenome-Wide Association StudyHumansMaleMendelian Randomization Analysis

Identifiers

PMID32366963
PMCPMC7198550

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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.