Effects of experimentally-induced diabetes on oestradiol-stimulated changes in the ultrastructure of the rat endometrium

Alterations in endometrial cell morphology following oestradiol treatment of ovariectomized animals were examined in euglycaemic and streptozotocin-induced diabetic rats. Endometrial morphology was examined 18, 24, 36 and 48 h after oestradiol administration. Nuclei of endometrial cells from saline injected euglycaemic and diabetic rats exhibited pleomorphic nuclei with areas of heterochromatin dispersed throughout the nucleus. Nuclei were homogenous in appearance and endometrial cells showed no mitotic chromosome function or cell division. The cytoplasm of euglycaemic and diabetic cells contained few mitochondria. The mitochondria that were present contained a uniformly dense matrix and cristae that extended across the mitochondria. The formation of round to oval shaped nuclei with diffuse euchromatin was observed at 18, 24 and 36 h following oestradiol administration in euglycaemic animals. Alterations in nuclear morphology and the formation of euchromatin were absent or reduced at the same time intervals examined in diabetic animals. Nucleoli in oestradiol-treated euglycaemic animals at 18, 24 and 36 h post-injections became very prominent and displayed easily visible granules and fibrillar material. Comparable changes in nucleolar morphology in oestradiol-treated diabetic rats were absent. The development of oval to round mitochondria containing short cristae and an electron-lucent matrix became apparent at 18 h post-injection of oestradiol in euglycaemic control animals. Alterations in mitochondrial morphology did not appear in endometrial cells of oestradiol-treated diabetic animals at any of the time points examined. At 24 and 36 h post-injection of oestradiol in euglycaemic animals, mitotic figures were observed in mitochondrial cells. Cell division and mitotic figures were not observed in oestradiol-treated diabetic animals. This study demonstrates that a diabetic state in experimental animals profoundly alters the ability of oestradiol to stimulate normal endometrial cell growth.