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Acetate supplementation restores testicular function by modulating Nrf2/PPAR-γ in high fat diet-induced obesity in
Kehinde S Olaniyi1,2, Christopher O Akintayo1, Adesola A Oniyide1
1Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, P.M.B. 5454, Ado-Ekiti, 360101 Nigeria.
Purpose:
Several 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.
Methods:
Adult male Wistar rats weighing 160-190 g were randomly allotted into three groups (n = 6/group): The groups received vehicle (distilled water), 40% HFD and sodium acetate (200 mg/kg) plus 40% HFD respectively. The administration lasted for 12 weeks.
Results:
HFD 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.
Conclusion:
The 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.
Insights
High-fat diets cause obesity and testicular dysfunction in rats. Acetate administration reversed these negative effects, improving testicular health by modulating key cellular pathways.
Area of Science:
- Reproductive biology
- Metabolic syndrome research
- Nutritional science
Background:
- Obesity is linked to impaired male reproductive function and infertility.
- Short-chain fatty acids (SCFAs) show potential in mitigating metabolic disorders.
- Understanding the impact of diet on testicular health is crucial for male fertility.
Purpose of the Study:
- To investigate if acetate, an SCFA, can counteract testicular dysfunction induced by a high-fat diet (HFD) in rats.
- To explore the role of Nrf2/PPAR-γ signaling in acetate's protective effects against HFD-induced testicular damage.
Main Methods:
- Adult male Wistar rats were fed a 40% HFD for 12 weeks.
- One group received sodium acetate (200 mg/kg) concurrently with the HFD.
- Control groups received either a vehicle or HFD alone.
Main Results:
- HFD induced obesity, insulin resistance, and testicular dysfunction, including lipid deposition, oxidative stress, and inflammation.
- HFD decreased levels of testicular antioxidants (glutathione, nitric oxide) and key regulatory proteins (Nrf2, PPAR-γ).
- Acetate treatment reversed HFD-induced testicular damage and normalized Nrf2 and PPAR-γ levels.
Conclusions:
- HFD-induced obesity leads to testicular dysfunction via lipid deposition, oxidative stress, and inflammation.
- Acetate administration can restore testicular function in obese rats.
- The beneficial effects of acetate are associated with the upregulation of Nrf2/PPAR-γ signaling pathways.
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