Estradiol-induced progesterone receptor synthesis in normal and diabetic ovariectomized rat uterus

Abstract

Estrogen stimulation of progesterone-receptor (Prog R.) synthesis is an important parameter of the sex hormones activity at the uterine level. Experimental diabetes in the rat has been shown to perturb protein synthesis in some tissues and to reduce, under certain circumstances, estrogen and androgen activity on their respective target tissues. The present work tended to evaluate the effect of steptozotocin diabetes on estradiol (E 2) stimulation of Prog. R and on Prog R. kinetics in the rat uterus. Two groups of diabetic rats were primed for three consecutive days with 5 microg. E 2 s.c. (EP). One group received an acute i.p. injection of progesterone (P), 1 h before sacrifice (Inj), the other group did not (n Inj). Two other groups, not primed with E 2 (nEP) were similarly injected or not with P. Four groups of non diabetic animals served as controls. Estrogen priming induced a 20–25% increase in DNA content, both in controls and in diabetics. Protein content was also increased to almost the same extent in diabetics and controls; protein concentration remained however slightly lower in cytosol of EP diabetics as compared to controls. Prog R. increased about 7-fold in cytosol and 4–5-fold in nuclei of EP control and diabetic groups. Cytosol to nuclei ratios of Prog R. decreased similarly in Inj. EP diabetics and controls, compared to the corresponcling n Inj. groups. It is concluded that estrogen priming stimulated Prog R., total protein and DNA synthesis to the same extent in diabetic as in control rats Prog R. kinetics was unaltered in diabetics. This fincling might be relevant to situations like early pregnancy, when Prog R. levels change rapidly and specifically in relation with the time and the site of implantation.