کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2062853 | 1076627 | 2008 | 16 صفحه PDF | دانلود رایگان |

SUMMARYPreviously, we found that in addition to embryos, the uterine tissues may be a source of estradiol-17β (E2) during early pregnancy in the pig. The aim of the present study was to determine whether porcine endometrium and myometrium secrete androgens - androstenedione (A4), testosterone (T) and estrone (E1) during early pregnancy and luteolysis (Days 14-16) in pigs. Individual endometrial and myometrial slices (200 mg) were first pre-incubated (24 h) and then incubated (6 h, 37°C in an atmosphere of 95% O2 and 5% CO2) in the presence or absence of progesterone (P4; 10−5 M), oxytocin (OT; 10−7 M) or OT plus P4. Basal endometrial and myometrial secretion of A4 and T did not differ between pregnant and cyclic gilts. Endometrial secretion of E1 was higher in pregnant than cyclic gilts (p<0.05) while myometrial secretion of E1 did not differ between the two groups of the examined pigs (p>0.05). Progesterone significantly increased A4 and T secretion (p<0.001) by uterine tissues regardless of the reproductive status. In the presence of P4, endometrial and myometrial secretion of E1 was increased only during luteolysis (p<0.001). In both tissues, OT did not affect the examined steroid secretion and did not change the effect of P4. In conclusion: 1) porcine endometrium and myometrium was found to produce A4, T and E1in vitro; 2) basal endometrial and myometrial production of A4 and T did not differ between the examined reproductive periods; 3) the endometrium released more E1 during early pregnancy than luteolysis; 4) in the presence of substrate (P4), uterine tissues increased secretion of A4 and T during early pregnancy and luteolysis; and 5) P4 increased uterine production of E1 only during luteolysis. These data demonstrated the presence of the active steroid pathway in porcine endometrium and myometrium which may serve as an alternative source of androgens and estrogens in pigs.
Journal: Reproductive Biology - Volume 8, Issue 3, November 2008, Pages 213–228