Observational studyScientific reports2025
Insulin resistance in polycystic ovary syndrome phenotypes and the vicious cycle model in its etiology.
Observational study in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Review
- Reduced CAG Repeats in the Androgen Receptor Gene May Independently Cause Polycystic Ovarian Syndrome.Current issues in molecular biology · 2026Review
- Development and temporal validation of a prediction model for live birth in infertile women with polyendocrine metabolic ovarian syndrome: a retrospective cohort study.Frontiers in reproductive health · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is a multifactorial disorder driven by at least three pathophysiological components: hypothalamic, ovarian, and obesity-related mechanisms. Insulin resistance (IR) is a unifying feature. Reciprocal interactions among androgen excess, hyperinsulinemia, and reduced hepatic sex hormone-binding globulin production create a self‑sustaining "vicious cycle" that exacerbates PCOS manifestations, which vary in severity and define four clinical phenotypes. To evaluate insulin resistance across PCOS phenotypes A (HA + OD + PCOM), B (HA + OD), C (HA + PCOM), and D (OD + PCOM). A retrospective observational study (2018-2022) of 200 Caucasian women aged 18-36 diagnosed with PCOS according to the Rotterdam criteria. Insulin resistance was assessed using HOMA‑IR. Clinical and anthropometric variables, Free Androgen Index (FAI), and Ferriman‑Gallwey (mFG) scores were analyzed by phenotype. Insulin resistance was present in 57.5% of participants. HOMA‑IR showed no correlation with PCOS duration but differed significantly between phenotypes. Mean HOMA‑IR values exceeded reference thresholds in all phenotypes: A 3.59, B 2.59, C 2.05, D 2.73. Moderate to strong positive correlations were observed between HOMA‑IR and mean arterial pressure, pulse rate, and waist‑to‑hip ratio, indicating an association with cardiometabolic risk across phenotypes. Positive associations among FAI, HOMA‑IR, and mFG score support a contribution of ovarian androgens to insulin resistance and hirsutism. Insulin resistance predominated in this PCOS cohort and was phenotype‑dependent rather than related to syndrome duration. All phenotypes exhibited elevated HOMA‑IR, with phenotype A showing the highest and phenotype C the lowest mean values. The proposed "vicious cycle" model integrates hyperandrogenism and hyperinsulinemia in peripheral insulin resistance; further research into genetic and intracellular signaling mechanisms is warranted.
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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 Socratic graph.