This study was designed to determine the effect of alloxan-induced (AI) and insulin resistant (IR) diabetes mellitus on gonadotropins and corpus luteum function in female rats. Female Sprague Dawley rats were randomly divided into 2 categories (non-pregnant and pregnant). Animals in each category were sub-divided into 3 groups. Group 1 served as control and were fed rat chow. Group 2 served as AI group and received alloxan i.v. into the tail vein (40 mg/kg) [1] at the 8th week. Group 3 served as IR group and were fed ad libitum on a special diet (25% fructose caked with 75% rat chow) for 12 weeks. Rats in both categories were surgically anaesthetized with ether, followed by laparatomy on the oestrus morning of the 12th week for removal of the ovaries in the non-pregnant category and laparatomy on day 19 of pregnancy for removal of the ovaries in the pregnant category. Blood was also obtained by cardiac puncture in both categories for measurement of serum LH, FSH, oestrogen and progesterone by radioimmunoassay. Rats in the pregnant category were mated at the end of the 12th week. The fetuses were weighed and the two ovaries processed for histological studies. Blood glucose concentration was significantly higher in the diabetic rats compared to control rats in both categories. In the non-pregnant category, body weight at the 10th and 12th week was significantly lower (P < 0.05) in AI and IR diabetic rats compared to control rats. In the pregnant category, it was not significantly different in the 3 groups throughout the trimesters of pregnancy. In the non-pregnant category, oestrous cycle was disrupted in the AI and IR groups. Serum FSH was significantly higher (P < 0.05) in AI diabetic rats only compared to control rats while serum LH, though higher in AI diabetic rats, was not significantly different when compared with the control rats. In the pregnant category, serum oestrogen was significantly higher (P < 0.05) in AI and IR diabetic pregnant rats compared to control pregnant rats. However, serum progesterone was not significantly different in the 3 groups. In both categories, absolute ovarian weight was significantly lower (P < 0.05) in AI and IR diabetic rats compared to control rats. Average fetal weight was significantly higher (P < 0.05) in IR diabetic pregnant rats compared to control and AI diabetic pregnant rats. Though fetal count was not significantly different in the 3 groups, resorption sites were significantly lower (P < 0.05) in AI and IR diabetic pregnant rats compared to control pregnant rats. Histological sections of ovaries show two or three corpora lutea as well as several follicles of varying sizes in the 3 groups. Follicles in AI and IR diabetic pregnant rats were cystically dilated and filled with pale eosinophilic fluid. Furthermore, the ovarian cysts in the IR diabetic pregnant rats were larger in size than those in the AI diabetic pregnant rats. These results show that diabetes mellitus alters serum gonadotropins and corpus luteum function in female rats. It also confirms that insulin resistance leads to macrosomia and predisposes to polycystic ovarian syndrome in rats.