Impact of Ovariectomy on the Anterior Pituitary Gland in Female Rats

Author:

Oride Aki1,Kanasaki Haruhiko1ORCID,Tumurbaatar Tuvshintugs1,Tumurgan Zolzaya1,Okada Hiroe1,Cairang Zhuoma1,Satoru Kyo1

Affiliation:

1. Department of Obstetrics and Gynecology, Shimane University School of Medicine, Izumo, Shimane 693-8501, Japan

Abstract

Ovariectomy (OVX) causes a depletion of circulating estradiol (E2) and influences hypothalamic kisspeptin neurons, which govern gonadotropin-releasing hormone (GnRH) release and ultimately gonadotropin secretion. In this study, we examined the changes induced by OVX on the anterior pituitary gland in female rats. OVX significantly increased the mRNA expression of gonadotropin α, luteinizing hormone (LH) β, and follicle-stimulating hormone (FSH) β subunits within the pituitary gland compared with control (sham-operated) rats, and this was completely suppressed by E2 supplementation. High-dose dihydrotestosterone supplementation also prevented the OVX-induced increase in the expression of the three gonadotropin subunits. GnRH receptor mRNA expression within the pituitary was significantly increased in OVX rats, and this increase was completely inhibited by E2 supplementation. The mRNA expression of the receptors for adenylate cyclase-activating polypeptide and kisspeptin was unchanged by OVX. Although the mRNA levels of inhibin α, βA, and βB subunits within the pituitary gland were not modulated by OVX, follistatin gene expression within the pituitary gland was increased by OVX, and this increase was completely inhibited by E2 supplementation after OVX. In experiments using a pituitary gonadotroph cell model (LβT2 cells), follistatin itself did not modulate the mRNA expression of gonadotropin LHβ and FSHβ subunits, and the GnRH-induced increase in the expression of these genes was slightly inhibited in the presence of follistatin. Our current observations suggest that OVX induces several characteristic changes in the pituitary gland of rats.

Funder

Ministry of Education, Culture, Sports, Science and Technology

Publisher

Hindawi Limited

Subject

Endocrine and Autonomic Systems,Endocrinology,Endocrinology, Diabetes and Metabolism

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