Kisspeptin in the hypothalamus of two rat models of polycystic ovary syndrome

• Published in: Endocrinology (Philadelphia) 2016-12, p.en.2016-1333
• Main Authors: Osuka, Satoko, Iwase, Akira, Nakahara, Tatsuo, Kondo, Mika, Saito, Ai, Bayasula, Nakamura, Tomoko, Takikawa, Sachiko, Goto, Maki, Kotani, Tomomi, Kikkawa, Fumitaka
• Format: Article
• Language: English
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/en.2016-1333

Hyperandrogenism, disturbance of the hypothalamus−pituitary−ovary axis followed by elevated serum luteinizing hormone (LH) levels, and insulin resistance are involved in the complicated pathophysiology of polycystic ovary syndrome (PCOS). Kisspeptin is co-expressed with neurokinin B (NKB) in the arcuate nucleus (ARC), the center of the gonadotropin-releasing hormone (GnRH)-pulse generator that is responsible for pulsatile LH secretion. We compared two androgenized rat models of PCOS to evaluate the estrous cycle, hormonal profiles, and expression of kisspeptin and NKB in the ARC. Rats in our postnatal dihydrotestosterone (DHT)-treatment model exhibited weight-gain and persistent diestrus with normal LH levels. In contrast, irregular cycles, with elevated LH serum levels and normal body weight, were found in the prenatally DHT-treated rats. We also found increased signals of kisspeptin and NKB in the ARC of the prenatally DHT-treated rats, and not in the postnatally DHT-treated rats. Our results suggest that prenatal exposure to androgens may result in higher kisspeptin and NKB levels in the ARC, which could be associated with one phenotype of PCOS characterized by normal body weight and higher LH secretion, while in postnatally DHT-treated rats, characteristics such as weight-gain and normal LH levels are seen in the obese PCOS phenotype.