ArticleJournal of diabetes and metabolic disorders2021
Acetate supplementation restores testicular function by modulating Nrf2/PPAR-γ in high fat diet-induced obesity in Wistar rats.
Article in Journal of diabetes and metabolic disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Ameliorative Effect of Policosanol on High-Fat Diet-Induced Testicular Dysfunction: Implications of ROS/SIRT1 and Apoptotic Signaling Pathways in Rats.Chemistry & biodiversity · 2026Article
- Article
- Changes in L-Carnitine Metabolism Affect the Gut Microbiome and Influence Sexual Behavior Through the Gut-Testis Axis.Microorganisms · 2025Article
- Immune Microenvironment Dysregulation: A Contributing Factor to Obesity-Associated Male Infertility.Biomedicines · 2025Review
- Lycopene alleviates 5-fluorouracil-induced nephrotoxicity by modulating PPAR-γ, Nrf2/HO-1, and NF-κB/TNF-α/IL-6 signals.Renal failure · 2024Article
- Thiazolidine-2,4-dione hybrids as dual alpha-amylase and alpha-glucosidase inhibitors: design, synthesis,RSC medicinal chemistry · 2024Article
- Article
- Sodium acetate ameliorates doxorubicin-induced cardiac injury via upregulation of Nrf2/HO-1 signaling and downregulation of NFkB-mediated apoptotic signaling in Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSeveral studies have established impaired testicular function in obese male population, including the young males with childhood obesity, contributing to increased male infertility, which is a universal trend in the last few decades. Short chain fatty acids (SCFAs) have been recently demonstrated to inhibit progression to metabolic comorbidities. The present study therefore hypothesized that SCFAs, acetate attenuates testicular dysfunction in high fat diet (HFD)-induced obese rat model, possibly by modulating Nrf2/PPAR-γ.
methodsAdult male Wistar rats weighing 160-190 g were randomly allotted into three groups (
resultsHFD caused obesity, which is characterized with increased body weight and visceral adiposity and insulin resistance/hyperinsulinemia. In addition, it increased testicular lipid deposition, malondialdehyde, pro-inflammatory mediators, lactate/pyruvate ratio, γ-Glutamyl transferase, and circulating leptin as well as decreased testicular glutathione, nitric oxide, Nrf2, PPAR-γ and circulating follicle stimulating hormone and testosterone without a significant change in testicular lactate dehydrogenase, blood glucose and luteinizing hormone when compared to the control group. Nevertheless, administration of acetate reversed the HFD-induced alterations.
conclusionThe present results demonstrates that HFD causes obesity-driven testicular dysfunction, associated with testicular lipid deposition, oxidative stress, and inflammation. The study in addition suggests the restoration of testicular function in obese animals by acetate, an effect that is accompanied by elevated Nrf2/PPAR-γ.
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