In the present study we wished to develop a model for polycystic ovari
an syndrome (PCOS) using the guinea pig, because this animal's cycle,
compared to other rodent models, more closely emulates that of humans.
Four silastic capsules, either empty or containing cholesterol or est
radiol-l7beta, were placed subcutaneously for 48 h on Day 10 or 12 of
the cycle. Vaginal smears were taken daily. Cardiac blood was drawn at
various intervals. At necropsy, trunk blood was collected and ovaries
were excised and analyzed histologically. Cycle length was extended o
ver that in controls in animals treated with estradiol-17beta (E2) on
Day 12 of the cycle. Treatment with E2 resulted in an increase in seru
m estrogen 2 h after capsule insertion. No changes were evident in pro
gesterone or androstenedione concentrations with treatment. Animals tr
eated with E2 and killed late (54 days after capsule removal) showed c
ysts grossly (group A), while occult cysts were present in E2-treated
animals killed early (17 days; group B); no cysts were observed in con
trol groups. Ovarian weight and size were increased in group A over co
ntrols. There was an increase in the fraction of atretic:total follicl
es < 500 mm in size in group A compared to group B as well as compared
to controls. Since these results are similar to those seen in human P
COS, we conclude that the guinea pig may serve as an exceptional and u
nique model for the study of PCOS and may be applicable to humans.