ArticleBMC pharmacology & toxicology2025
Quercetin-mediated restoration of high-fat diet-induced male reproductive dysfunction through modifying spermatogenesis and unraveling 3β-HSD, 17β-HSD, and StAR pathways.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Characterization, Analysis, and Alleviating Effects of Sulfated Polysaccharides Derived From Agardhiella subulata on Di-(2-Ethylhexyl) Phthalate-Induced Testicular Toxicity in Mice.Molecular nutrition & food research · 2026Article
- Beta-caryophyllene mitigates high fat diet-induced testicular dysfunctions by targeting JNK/ERK-1 and JAK-1/STAT-3 pathways in rats.Scientific reports · 2026Article
- Reproductive and immune-related consequences ofFrontiers in veterinary science · 2026Article
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Authors and funding
3 authors.
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Abstract
purposeWe explored the astounding potential of quercetin (QRT) to counteract the determinantal impacts of a high-fat diet (HFD) on testicular function in rat model. The goal was to understand how QRT, and its mechanisms of action can protect testicular health from HFD.
methodsRats were divided into four groups receiving a control diet, QRT supplement (100 mg/kg), HFD, or HFD plus QRT for 8 weeks. Afterward, assessments were conducted, and reproductive organs were analyzed for hormone levels, gene expression, and subjected to biochemical, histopathological, and immunohistochemical analyses.
resultsThe HFD caused substantial declines in testicular weight, accessory sex glands and epididymis. The HFD also negatively impacted sperm characteristics including reduced motility, viability, and count, along with impaired morphology. Additionally, the HFD decreased testosterone levels in the testes and serum, impaired antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase, and reduced expression of key steroid metabolism enzymes 17β-hydroxysteroid dehydrogenase (17β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), and steroidogenic acute regulatory protein (StAR) involved in testosterone synthesis. These changes were paired with enhanced testicular lipid peroxidation, nitrite, and the inflammatory marker tumor necrosis factor-alpha (TNF-α), reflecting the damaging еffеcts of the HFD. Examination of testicular tissues verified structural damage and significantly fewer proliferating cell nuclear antigen (PCNA)-positive spermatogenic cells in seminiferous tubules of HFD-fed group, confirming HFD's adverse еffеcts.
conclusionQRT supplementation was able to curb the harmful impacts of the HFD on testicular spermatogenesis and steroidogenesis through its antioxidant, anti-inflammatory and androgen boosting properties.
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