<p>Asprosin, a fasting-induced adipokine, has been reported to exhibit altered circulating levels in women with polycystic ovary syndrome (PCOS); however, its tissue-specific regulation and the role of its receptor, OLFR734, in PCOS remain poorly understood. In this study, we present the first histological evidence of asprosin and OLFR734 expression in reproductive tissues using dehydroepiandrosterone-induced PCOS mouse models maintained on chow or a high-fat diet (HFD). Metabolic profiling revealed distinct phenotypes, with HFD-fed PCOS mice showing pronounced metabolic disturbances, including increased body weight, glucose intolerance, dyslipidemia, and elevated serum asprosin levels, compared with chow-fed PCOS mice. Asprosin was immunodetected in adipose tissue, ovary, oviduct, and uterus, with increased expression in both PCOS groups. In control ovaries, asprosin was restricted to the theca layer of Graafian follicles. In contrast, PCOS ovaries showed distinct asprosin expression patterns in the theca, granulosa cells, and the antrum of cystic follicles. Asprosin-positive cells were also observed in the oviduct and uterus, with distinct uterine localization in PCOS. OLFR734 showed a similar broad tissue distribution to asprosin, with upregulated expression in both PCOS diet groups. Notably, androgen excess and dietary fat exposure did not produce uniform or additive effects on tissue-level asprosin-OLFR734 expression but instead revealed tissue-specific response patterns under different dietary conditions. Collectively, our findings suggest a potential association of the asprosin-OLFR734 axis with reproductive changes in PCOS, linking metabolic and reproductive dysfunction under diet-induced stress. This work provides a histological and comparative framework, highlighting asprosin and OLFR734 as emerging molecular candidates in PCOS that warrant further investigation for their potential roles in disease pathophysiology.</p>