SynthesisBMC endocrine disorders2025
Effects of Genistein on polycystic ovary syndrome of rats: a systematic review and meta-analysis.
Synthesis in BMC endocrine disorders, 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.
- Exploring the Health Effects of Phytoestrogens.Metabolites · 2026Review
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
Abstract
backgroundPCOS is a complex endocrine-metabolic disorder that is closely associated with oxidative stress. GEN, a naturally occurring isoflavone, has demonstrated beneficial effects in addressing hormonal imbalances and metabolic disturbances, primarily due to its potent antioxidant properties. While accumulating evidence supports its potential in managing PCOS, the full extent of GEN's therapeutic efficacy in alleviating PCOS-related symptoms remains inadequately defined, warranting further detailed investigation. PURPOSE: This study aims to systematically evaluate the pharmacological efficacy of GEN in the management of PCOS through a meta-analytic synthesis of preclinical data.
methodsA comprehensive literature search was conducted across six major databases-CNKI, Wanfang Data, VIP, PubMed, and Web of Science-covering publications from database inception until May 2025. The methodological quality of eligible studies was assessed using SYRCLE's risk of bias tool. Data synthesis and meta-analysis were performed using Rev Man 5.3 and Stata 17 software to ensure statistical analysis of the pooled outcomes.
resultsA total of ten studies were included in the meta-analysis. Compared to the control group, GEN exhibited significant therapeutic effects in the treatment of PCOS, including a reduction in body weight (P < 0.00001) and ovarian weight (P < 0.00001) in PCOS rats, as well as a reversal of elevated serum levels of T (P = 0.003) and LH (P < 0.00001). GEN also significantly reduced FBG (P = 0.007), INS (P = 0.0006), and HOMA-IR indices (P = 0.01), decreased MDA content (P = 0.0002) in ovarian tissue, and enhanced antioxidant activity, as indicated by increases in TAC (P < 0.00001), SOD (P < 0.00001), and GPx (P = 0.02). Furthermore, GEN lowered serum levels of LDL-C (P < 0.00001).
conclusionGEN demonstrates considerable therapeutic potential in managing PCOS through multiple mechanisms. These include modulation of body and ovarian weight, restoration of endocrine balance by reducing hyperandrogenism and normalizing reproductive hormone profiles, improvement of metabolic parameters through enhanced insulin sensitivity and glycemic control, and attenuation of oxidative stress via increased antioxidant enzyme activity and reduction of lipid peroxidation markers. These findings emphasize GEN's promise as a multifaceted intervention for PCOS, underscoring the need for further translational research to confirm its clinical efficacy.
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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 OpenQuestion graph.