垂体促性腺激素直接控制卵巢功能,而这些激素又受卵巢类固醇激素的调节。促性腺激素和类固醇激素的精确相互作用对于卵泡生长和分化至关重要。此外,自噬调节卵泡分化。然而,高脂高果糖(HFD-HF)饮食如何调节促性腺激素和促进自噬介导的卵巢卵泡分化尚不清楚.我们给青春期前大鼠(PND25)喂食HFD-HF饮食,直到PND90。结果显示腺垂体GnRHR减少,PR,和芳香化酶表达,而AR,ERα,PRLR,抑制素增强了,导致促性腺激素下降。有趣的是,自噬生物标志物,Beclin-1,ATG5,ATG12,LC3-II,和LAMP1减少,但SQSTM1/p62在HFD-HF喂养大鼠的卵巢中增加,导致自溶体聚集。饮食改变了T,E2,P4,PRL,以及它们在卵巢中的受体状态,受扰的动情周期,阴道开放延迟。卵巢组织形态学表现出许多囊性和闭锁性卵泡,伴随着卵泡成熟和排卵的紊乱。此外,FSHR的减少;类固醇生成蛋白;受体蛋白AR,ERβ,PR;和信号蛋白Wnt2和β-catenin也在卵巢中被发现,而PRLR,抑制素,pGSK3β增强。总之,暴露于青春期前HFD-HF饮食会导致促性腺激素减退和自噬介导的卵巢卵泡分化缺陷,降低成年大鼠的生育能力。
Pituitary gonadotropins directly govern ovarian functions, which are in turn regulated by the ovarian steroid hormones. The precise interplay of gonadotropins and steroid hormones is critical for follicle growth and differentiation. Furthermore, autophagy regulates ovarian follicle differentiation. However, how the high-fat-high fructose (HFD-HF) diet regulates gonadotropins and facilitates autophagy-mediated follicular differentiation in the ovary is obscure. We fed prepubertal rats (PND 25) an HFD-HF diet until PND 90. The results showed diminished adenohypophyseal
GnRHR, PR, and aromatase expression, whereas AR, ERα, PRLR, and inhibin were augmented, resulting in gonadotropins decline. Interestingly, autophagy biomarkers, Beclin-1, ATG5, ATG12, LC3-II, and LAMP1 were reduced but SQSTM1/p62 was augmented in the ovaries of HFD-HF-fed rats, causing autolysosome to aggregation. The diet altered T, E2, P4, PRL, and their receptors status in the ovary, disturbed estrous cyclicity, and delayed vaginal opening. Ovarian histomorphology exhibited numerous cystic and atretic follicles, along with disturbed follicular maturation and ovulation. Moreover, the reduction of FSHR; steroidogenic proteins; receptor proteins AR, ERβ, PR; and signaling proteins Wnt2 and β-catenin was also noticed in the ovary, whereas PRLR, inhibin, and pGSK3β were augmented. In conclusion, exposure to a prepubertal HFD-HF diet leads to hypogonadotropism and the autophagy-mediated defective differentiation of ovarian follicles, abating fertility in adult rats.