Abstract
(1) Background: In recent decades, the prevalence of obesity has grown rapidly worldwide, thus causing many diseases, including male hypogonadism. Sulforaphane (SFN), an isothiocyanate compound, has been reported to protect the reproductive system. This research investigated the protective effect of SFN against obesity-induced impairment in the male reproductive system and explored the potential mechanism involved in mice. (2) Methods: One hundred thirty mice were divided into 5 groups (Control, DIO (diet-induced obesity), DIO + SFN 5 mg/kg, DIO + SFN 10 mg/kg, and DIO + SFN 20 mg/kg). The effects of SFN on the male reproductive system were determined based on the sperm count and motility, relative testes and epididymis weights, hormone levels, and pathological analyses. Oxidative stress was determined by measuring malondialdehyde (MDA), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione (GSH), H2O2, catalase (CAT), and glutathione peroxidase (GSH-PX) levels. Protein expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Kelch-like ECH-associated protein-1 (Keap1), Microtubule-associated protein light chain 3 (LC3), Beclin1, and P62 were determined by western blotting. (3) Results: High-fat diet (HFD)-induced obesity significantly decreased relative testes and epididymis weights, sperm count and motility, and testosterone levels but increased leptin and estradiol levels. SFN supplementation ameliorated these effects. Additionally, SFN administration inhibited the obesity-induced MDA accumulation and increased the SOD level. Western blot indicated that SFN had an important role in the downregulation of Keap1. Moreover, SFN treatment attenuated obesity-induced autophagy, as detected by LC3 and Beclin1. (4) Conclusions: SFN ameliorated the reproductive toxicity associated with obesity by inhibiting oxidative stress mediated by the nuclear factor erythroid-2 related factor 2/ antioxidant response element (Nrf2/ARE) signaling pathway and recovery of normal autophagy.
Highlights
Obesity, which is a metabolic disease, is generally considered to be associated with heredity, behavior, environment, and so on
SFN 10 mg/kg (28.95 ± 0.86 g), and Diet-Induced Obesity (DIO) + SFN 20 mg/kg (28.21 ± 0.65 g) groups were higher than the body weight of controls (26.98 ± 1.40 g; p < 0.01; Figure 3)
We discovered that obesity increased the expression of Kelch-like ECH-associated protein-1 (Keap1) and decreased levels of nuclear factor erythroid-2 related factor 2 (Nrf2) as well as the activation of other antioxidant enzymes, indicating that obesity-induced oxidative stress improved by stimulation of the Nrf2 antioxidant pathway
Summary
Obesity, which is a metabolic disease, is generally considered to be associated with heredity, behavior, environment, and so on. The prevalence of obesity is continuing to increase at an alarming rate and has nearly tripled in the last 40 years [1]. In 2016, the prevalence of obesity among adults was. 13% and the morbidity of overweight adults was 39% worldwide. The overweight and obesity rates among children and adolescents rose from 4% in 1975 to 18% in 2016 [2]. Studies have shown that obesity can affect paternal reproduction [3]. The sperm count or motility are decreased and sperm DNA is damaged in men who are obese or overweight compared to men with normal BMI [4,5].
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