Evidence map›Paper›PMID 40315335›Full record

ArticleEuropean journal of endocrinology2025

Genetic predisposition to adiposity, and type 2 diabetes: the role of lifestyle and phenotypic adiposity.

Mengrong Zhang, Joey Ward, Rona J Strawbridge, Jana J Anderson, Carlos Celis-Morales, Jill P Pell, Frederick K Ho, Donald M Lyall

Abstract read
In one paragraph

Article in European journal of endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. The CommonNutrients · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
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

8 authors.

Mengrong ZhangSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.ORCID 0009-0005-2391-4416
Joey WardSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.
Rona J StrawbridgeSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.
Jana J AndersonSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.ORCID 0000-0001-7290-6635
Carlos Celis-MoralesSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.
Jill P PellSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.
Frederick K HoSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.
Donald M LyallSchool of Health and Wellbeing, University of Glasgow, Glasgow G12 8TB, United Kingdom.ORCID 0000-0003-3850-1487

Funding

British Heart FoundationChina Scholarship CouncilDepartment of HealthHDR-UK MR/S003061/1Medical Research CouncilScottish Government and Northwest Regional Development AgencyUKBWellcome TrustWelsh Assembly Government
6 · The paper itself

Abstract

aimsGenetic predisposition to adiposity is associated with type 2 diabetes (T2D), even in the absence of phenotypic adiposity (obesity and central obesity). We aimed to quantify the overall contribution of obesity and modifiable lifestyle factors to the association between genetic predisposition to adiposity and the development of T2D.

methodsThis prospective cohort study involved 220 703 White British participants from the UK Biobank. It examined the associations between genetic predisposition to adiposity [body mass index polygenic risk (BMI-PRS) and waist-hip ratio polygenic risk (WHR-PRS)] and incident T2D, as well as interactions and mediation via lifestyle factors (diet quality, physical activity levels, total energy intake, sleep duration, and smoking and alcohol intake) and phenotypic adiposity.

resultsPeople with high phenotypic adiposity and high adiposity PRS values (>1 SD above the mean) had the highest risk of incident T2D (versus non-obese/central obese and non-high PRS). This was the case for BMI-PRS [hazard ratio (HR) = 3.72] and WHR-PRS (HR = 4.17). Lifestyle factors explained 30.5% of the BMI-PRS/T2D association (2.0% mediation; 28.5% effect modification), and lifestyle and obesity together explained 92.1% (78.8% mediation; 13.3% effect modification). Lifestyle factors explained 20.4% of the WHR-PRS/T2D association (3.4% mediation; 17.0% effect modification), and lifestyle and central obesity together explained 72.8% (41.1% mediation; 31.7% effect modification).

conclusionsWhilst phenotypic adiposity explains a large proportion of the association between BMI-PRS/WHR-PRS and T2D, modifiable lifestyle factors also make contributions. Promoting healthy lifestyles among people prone to adiposity is important in reducing the global burden of T2D.

Indexed as

AdiposityDiabetes Mellitus, Type 2Genetic Predisposition to DiseaseLife StyleObesityAdultAgedBody Mass IndexCohort StudiesExerciseFemaleHumansMaleMiddle AgedPhenotypeProspective StudiesadiposityBMI-PRScentral obesitylifestyle factorsobesityT2DWHR-PRS

Identifiers

PMID40315335
PMCPMC12056655

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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.