Asset Details
Do you wish to reserve the book?
Adiposity, metabolites and endometrial cancer risk: inference from combinations of Mendelian randomization and observational analyses
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Adiposity, metabolites and endometrial cancer risk: inference from combinations of Mendelian randomization and observational analyses
Do you wish to request the book?
Adiposity, metabolites and endometrial cancer risk: inference from combinations of Mendelian randomization and observational analyses
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Adiposity, metabolites and endometrial cancer risk: inference from combinations of Mendelian randomization and observational analyses
2025
Overview
Introduction
The associations between excess adiposity and endometrial cancer (EC) risk may be mediated by altered metabolic profiles. Here, we triangulated evidence from observational and Mendelian randomisation (MR) analyses to investigate the relationship between adiposity traits, circulating metabolites, and their effects on endometrial cancer.
Methods
Observational analyses were performed in UK Biobank (N cases and controls = 1,005 and 215,339, respectively). Univariable and multivariable MR analyses were performed using female-specific summary statistics for adiposity traits (GIANT consortium; N BMI and WHR = 434,793 and 281,153, respectively), circulating metabolites (UK Biobank;
N
= 140,768) and EC (Endometrial Cancer Association Consortium; N cases and controls = 12,906 and 108,979, respectively).
Results
Higher body mass index (BMI) was associated with increased odds of overall EC, endometrioid EC, and non-endometrioid EC in both observational and MR analyses; however, there was weaker evidence for waist-hip-ratio (WHR). BMI was associated with 165 metabolites, 25 of which were associated with EC risk. Multivariable MR analyses suggest that several lipid metabolites and ratios may mediate the association between BMI and non-endometrioid EC, although analyses using Phenoscanner suggest that alternative pathways such as height and blood cell traits could influence the EC risk.
Conclusion
Evidence here suggests that higher BMI causes a higher risk of overall and all histological subtypes of EC and variation in numerous circulating metabolites. Several of these metabolites showed relationships consistent with an intermediate role between BMI and non-endometrioid EC, however, further analyses highlighted other potential shared mechanisms that could influence the risk of EC.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Age
/ Analysis
/ Biobanks
/ Biomedical and Life Sciences
/ Endometrial Neoplasms - epidemiology
/ Endometrial Neoplasms - etiology
/ Endometrial Neoplasms - genetics
/ Endometrial Neoplasms - metabolism
/ Exercise
/ Female
/ Females
/ Genomes
/ Health Promotion and Disease Prevention
/ Humans
/ Mendelian Randomization Analysis
/ NMR
/ Oncology
/ Ratios
