ArticleAndrology2026
Comprehensive Quantification of Oligoasthenozoospermia Induced by Obesity, Reproductive Toxicants, and Their Combination in Rat Models.
Article in Andrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundOligoasthenozoospermia is a leading cause of male infertility and has been increasingly associated with the global surge in obesity and exposure to reproductive toxicants. Despite extensive research on each factor individually, their combined pathological effects remain poorly understood.
objectivesThis study aimed to investigate how obesity and reproductive toxicants independently and synergistically impair male reproductive function by establishing and comparing rat models of oligoasthenozoospermia induced by each factor and their combination. MATERIALS AND
methodsWe constructed three etiologically distinct oligoasthenozoospermia male Sprague-Dawley rat models: a reproductive toxicity model induced by glycosides of Tripterygium wilfordii Hook. f. (GTW), a metabolic dysfunction model induced by a high-fat diet (HFD), and a combined model (HFD + GTW). Animals were randomly assigned and subjected to 12 weeks of treatment. Body weight, metabolic indices, serum sex hormone levels, sperm quality parameters, and histopathological analysis of the testes and epididymis, as well as gut microbiota composition and testicular transcriptome profiles, were systematically evaluated. We also performed quantitative real-time polymerase chain reaction.
resultsBoth GTW and HFD independently impaired reproductive function, leading to decreased sperm count and motility, hormonal disturbances, and moderate testicular damage. The combined model exhibited significantly exacerbated reproductive impairment, including extensive spermatogenic cell loss, disrupted testicular architecture, and the lowest sperm quality indices. Multiomics analysis revealed coordinated alterations in gut microbiota composition and testicular transcriptomes, suggesting crosstalk between metabolic and inflammatory signaling pathways. Quantitative real-time polymerase chain reaction confirmed these transcriptomic patterns, showing upregulation of Ahnak, C1r, S1pr1, and Steap4, alongside downregulation of Alkbh7, Tbpl1, Tent5b, and Ldhal6b in the models.
conclusionThis study successfully establishes reliable rat models that mimic both individual and combined etiologies of oligoasthenozoospermia. The interaction between obesity and GTW-induced reproductive toxicity aggravates testicular injury through metabolic disruption and inflammatory pathways, offering an integrative platform for mechanistic and therapeutic research.
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.