Unveiling the intricate hormonal regulation of asprosin and its receptor in the mice testis

Asprosin is reported to regulate testicular functions directly as well as through the modulation of gonadotropin and sex steroid levels; however, hormonal regulation of testicular asprosin and its receptor, Olfr734, remains unexplored. The present in vitro study for the first time demonstrates that gonadotropins and corticosterone inhibit expression of both asprosin and its receptor, while sex steroids and insulin stimulate asprosin but suppress Olfr734 in mice testis.

Asprosin, a recently discovered adipokine, has emerged as a modulator of gonadal functions. In males, asprosin stimulates testicular functions such as spermatogenesis, steroidogenesis, and energy metabolism. It is reported to employ olfactory receptor 734 (OLFR734) to stimulate progressive sperm motility. However, investigations exploring the hormonal regulation of testicular asprosin are completely lacking. Hence, the current study aims to explore the effect of different hormones on testicular expression of asprosin and its receptor, Olfr734, in mice. Adult mice testes were excised and subjected to in vitro treatment (12 h) with different concentrations of gonadotropins (luteinizing hormone, LH, and follicle-stimulating hormone, FSH), sex steroids (dihydrotestosterone, DHT, and estradiol, E2), and metabolic hormones (corticosterone and insulin). Post-incubation, testes were processed for total RNA and protein extraction. The mRNA expression of asprosin (Fbn1) and Olfr734 was quantified using quantitative real-time polymerase chain reaction, while the asprosin protein expression was assessed using western blotting. Our results revealed that gonadotropins (LH and FSH) inhibited the expression of asprosin (Fbn1) and Olfr734. On the contrary, sex steroids upregulated testicular asprosin while downregulating Olfr734. Insulin-treated testes also demonstrated increased expression of asprosin, indicating a positive correlation between the two. Interestingly, Olfr734 expression was suppressed by insulin. Furthermore, the stress hormone corticosterone inhibited expression of both asprosin and Olfr734. This study provides the first evidence of hormonal regulation of testicular asprosin and its receptor, Olfr734, possibly functioning to ensure optimal testicular functions in mice.