Expression of Luteinizing Hormone (LH) Receptor Gene in the Ovary of a Prenatally-Androgenized Rat Model of Polycystic Ovary Syndrome Following Androgen Exposure in the Prenatal Period

Based on available evidence, exposure of the female fetus to androgens during the prenatal period, by affecting the expression of some genes, can cause polycystic ovary syndrome (PCOS) in adulthood. On the other hand, changes in luteinizing hormone (LH) levels and its receptor are associated with the risk of reproductive disorders, including PCOS. The present study aimed to evaluate the expression of the LH receptor gene in the ovaries of a rat model of PCOS induced by androgen exposure in the prenatal period.

In adult rats with PCOS and controls (eight animals in each group), different phases of the sexual cycle (estrous cycle) were determined using vaginal smears, and the anogenital distance (AGD) was measured using a vernier caliper. Ovarian granulosa cells were isolated, and RNA was extracted. The LH receptor gene expression levels in these cells were determined using the real-time polymerase chain reaction (PCR). Data were analyzed by GraphPad Prism software.

Irregular and longer sexual cycles, an increase in AGD (17.32 17 0.3 vs. 11.73 ± 0.26 mm (P=0.0001)), and a decrease in LH receptor gene expression (42. ± 0.12) 0 vs. 0.88 (0.13 (P=0.02)) were observed in the adult rat model of PCOS compared to controls.

A decrease in LH receptor gene expression in the ovarian granulosa cells may be one of the mechanisms involved in the pathophysiology of PCOS following prenatal exposure of the female fetus to androgens.