Diet-induced
obesity has been associated with various metabolic and reproductive disorders, including
polycystic ovary syndrome. However, the mechanisms by which
obesity influences the reproductive system are still not fully known. Studies have suggested that impairments in
hormone signaling are associated with the development of symptoms such as acyclicity and
ovarian cysts. However, these studies have often failed to address how these hormonal changes arise and how they might contribute to the progression of reproductive diseases. In the present study, we used a high-fat, high-
sugar (HFHS) diet to induce
obesity in a female rodent model to determine the changes in critical reproductive
hormones that might contribute to the development of irregular estrous cycling and reproductive cycle termination. The HFHS animals exhibited impaired
estradiol,
progesterone (P4), and
luteinizing hormone (LH) surges before ovulation. The HFHS diet also resulted in altered basal levels of
testosterone (T) and LH. Furthermore, alterations in the basal P4/T ratio correlated strongly with
ovarian cyst formation in HFHS rats. Thus, this model provides a method to assess the underlying etiology of
obesity-related reproductive dysfunction and to examine an acyclic reproductive phenotype as it develops.