article · Chemistry & Biodiversity
Consuming a high-fat diet can cause testicular dysfunction through hormonal disturbances, sperm abnormalities, and severe metabolic disruption. In a laboratory study using rats, a high-fat diet induced notable weight gain, insulin resistance, abnormal lipid levels, inflammation, and excess reactive oxygen species in testicular tissue. It also disrupted key cellular protection mechanisms by reducing SIRT1, Nrf2, and HO-1 levels, whilst elevating markers associated with cell death and autophagy. Oral treatment with policosanol at a dose of 10 mg/kg per day for four weeks reversed these harmful changes. The natural compound improved overall metabolic status, reduced oxidative stress and inflammation, and normalised apoptotic signalling pathways. These findings indicate that policosanol counteracts diet-induced testicular damage by activating protective SIRT1, Nrf2, and HO-1 pathways.
Dietary habits and obesity can negatively impact male reproductive health by causing cellular damage and metabolic disorders. Understanding how natural compounds such as policosanol alleviate oxidative stress and regulate cellular survival pathways offers potential routes for protecting against diet-related testicular dysfunction and supporting reproductive wellbeing.
This work identifies policosanol as a potential therapeutic candidate for managing diet-induced testicular dysfunction and related metabolic harm. It could be relevant to pharmaceutical and nutraceutical developers focused on male reproductive health and metabolic disorders. Because the evidence is derived entirely from an in vivo animal model, the research remains at an early stage, requiring extensive clinical validation before commercial applications can be realised.
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High-fat diet (HFD) intake may lead to testicular dysfunction, mostly attributed to hormonal disturbances and spermatozoa deformities. The present study was designed to demonstrate the policosanol (POL) effect on testicular dysfunction due to HFD intake. Rats were randomly divided into three groups; one received HFD for 16 weeks and then treated with POL (10 mg/kg/day) orally for 4 weeks along with HFD intake. The second group received HFD only and served as the HFD control group. The third group was referred to as normal control (NC) and kept on a normal chow diet. Rats subjected to HFD showed marked weight gain, dyslipidemia, insulin resistance, excessive generation of reactive oxygen species (ROS) and inflammation status. Silent information regulator transcript-1 (SIRT1) protein levels and mRNA expression levels of nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) showed significant decrease in the HFD group. Bax and caspase-3, along with Beclin-1, showed substantial increases along with Bcl-2 decrease. POL administration successfully reversed all these abnormalities which may be attributed to activation of SIRT1/Nrf2/HO-1 signaling. Collectively, POL administration may be a promising therapeutic approach against HFD-testicular dysfunction via improving metabolic status, attenuating oxidative stress and inflammation, and modulating apoptosis and autophagy.
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DOI: 10.1002/cbdv.71345
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