Maternal diabetes is known to impair placental function; however, its effect on placental expression of progesterone and oestrogen receptors has not been well documented. Fructose has been used to induce insulin resistance in animal models (Suga et al., 2000). The study aimed to assess maternal serum levels of progesterone, oestriol, oestradiol; placental morphology and its expression of progesterone and oestrogens receptors in fructose-induced diabetic rats. Twelve female rats were randomly divided into two groups namely group 1; control rats fed with normal rat chow and group 2; treated rats fed a diet consisting of 25% fructose to induce type 2 diabetes mellitus. Hyperglycaemia and hyperinsulinemia were confirmed after 8 weeks of fructose feeding. Rats in both groups were mated and pregnancy confirmed. Blood samples were obtained and assessed for glucose, insulin, progesterone, oestriol and oestradiol levels. Placental tissues were isolated, weighed and fixed for morphological studies and the expression of oestrogens and progesterone receptors using immunohistochemical technique. Results showed that blood glucose, insulin and progesterone levels were significantly increased in the diabetic rats with no significant difference in oestriol and oestradiol levels. Placental weight, central thickness and diameter were increased; placental junctional zones were enlarged due to an increase in the number of glycogen and trophoblast giant cells in the diabetic placentae. Progesterone receptor expression was down regulated in the placentae of diabetic rats, while there was no significant difference in oestrogens receptor expression compared to the control placentae. Type 2 diabetes mellitus therefore increases progesterone levels, impairs placental morphology and down regulates placental progesterone receptor expression in pregnant rats.
Keywords: placenta, diabetes, pregnancy
Reference: Suga, A., Hirano, T., Kageyama, H. (2000). Effects of fructose and glucose on plasma leptin, insulin and insulin resistance in lean and VMH lesioned obese rats. American Journal of Physiology-Endocrinology and Metabolism, 278(4): E677E683.