ArticleInternational journal of women's health2025
Beyond BMI: A Mendelian Randomization Study of the Causal Effects and Mediating Pathways of Regional Adipose Tissue Depots on Polycystic Ovary Syndrome.
Article in International journal of women's health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- PMOS in black girls and women: from high to low risk.Journal of endocrinological investigation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous studies suggest that increased body fat is associated with polycystic ovary syndrome (PCOS) risk. Recent evidence highlights that the distribution of adipose tissue may play a more critical role in predicting PCOS risk compared to total fat mass; however, causal relationships remain unclear. This Mendelian randomization (MR) study aimed to investigate the causal associations between body mass index (BMI)-independent regional adipose tissue distribution and PCOS risk. Methods: Female-specific data on regional adipose tissue depots (n Results: Genetically predicted higher GFAT volume demonstrated a significant causal protective effect on PCOS risk (OR = 0.845, 95% CI: 0.735-0.971). This protective effect was predominantly mediated through reductions in fasting insulin (58.37%, 95% CI: 27.66-89.08%) and leptin (51.75%, 95% CI: 33.54-75.41%). Other mediators included the homeostasis model assessment of insulin resistance (HOMA-IR; 37.20%), sex hormone-binding globulin (SHBG; 24.74%), bioavailable testosterone (BT; 11.99%), and triglycerides (TG; 9.52%). Additionally, suggestive evidence driven by a single genetic instrument linked higher VAT/ASAT, VAT/GFAT, and ASAT/GFAT ratios to increased PCOS risk (OR > 1). Sensitivity analyses and supplementary methods confirmed the robustness of these findings. Conclusion: This study provides causal evidence supporting the protective role of GFAT against PCOS and identifies critical metabolic and hormonal pathways as mediators. These results highlight the significance of adipose tissue distribution patterns in the pathogenesis of female endocrine disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.